Abstract: OBJECTIVE: To evaluate the usefulness of systematic coronary angiography followed, if needed, by coronary artery angioplasty (percutaneous coronary intervention (PCI)) on the incidence of cardiac ischaemic events after carotid endarterectomy (CEA) in patients without evidence of coronary artery disease (CAD). MATERIALS AND METHODS: From January 2005 to December 2008, 426 patients, candidates for CEA, with no history of CAD and with normal cardiac ultrasound and electrocardiography (ECG), were randomised into two groups. In group A (n=216) all the patients had coronary angiography performed before CEA. In group B, all the patients had CEA without previous coronary angiography. In group A, 66 patients presenting significant coronary artery lesions at angiography received PCI before CEA. They subsequently underwent surgery under aspirin (100 mg day(-1)) and clopidogrel (75 mg day(-1)). CEA was performed within a median delay of 4 days after PCI (range: 1-8 days). Risk factors, indications for CEA and surgical techniques were comparable in both groups (p>0.05). The primary combined endpoint of the study was the incidence of postoperative myocardial ischaemic events combined with the incidence of complications of coronary angiography. Secondary endpoints were death and stroke rates after CEA and incidence of cervical haematoma. RESULTS: Postoperative mortality was 0% in group A and 0.9% in group B (p=0.24). One postoperative stroke (0.5%) occurred in group A, and two (0.9%) in group B (p=0.62). No postoperative myocardial event was observed in group A, whereas nine ischaemic events were observed in group B, including one fatal myocardial infarction (p=0.01). Binary logistic regression analysis demonstrated that preoperative coronary angiography was the only independent variable that predicted the occurrence of postoperative coronary ischaemia after CEA. The odds ratio for coronary angiography (group A) indicated that when holding all other variables constant, a patient having preoperative coronary angiography before carotid surgery was 4 times less likely to have a cardiac ischaemic event after carotid surgery. No complications related to coronary angiography were observed and no cervical haematomas occurred in patients undergoing surgery under aspirin and clopidogrel in this study. CONCLUSIONS: Systematic preoperative coronary angiography, possibly followed by PCI, significantly reduces the incidence of postoperative myocardial events after CEA in patients without clinical evidence of CAD.
Abstract: BACKGROUND: Interventional treatment with atorvastatin lowered the circulating levels of the catalytic core of NADPH oxidase, namely sgp91(phox), but the underlying mechanism is still undefined. AIM: To test the hypothesis that the inhibitory effect on oxidative stress, induced by Atorvastatin, could be mediated by adiponectin. METHODS AND RESULTS: We compared 36 patients with polygenic hypercholesterolemia and 18 healthy subjects. Patients were randomized to either a low-fat diet (Group A) or low-fat diet plus atorvastatin 10 mg/day (Group B) for 30 days. Lower serum adiponectin levels and higher lipid profile, gp91(phox) serum levels, urinary isoprostanes, platelet oxygen free radicals, characterized patients. After 30 days of treatment, group B showed higher levels of adiponectin which is inversely correlated to reduced levels of sgp91(phox), urinary isoprostanes and platelet oxygen free radicals (p<0.001). In in vitro model, adiponectin dosages between 5 and 10 ng/ml inhibited p47(phox) translocation to gp91(phox) and soluble gp91(phox) cleavage indicating its ability in inhibiting the assembly of NADPH oxidase subunits on cell membrane and in turn the enzymatic system activation. CONCLUSION: This study provides the first evidence that in patients higher APN serum levels are associated with gp91(phox) down-regulation. APN-mediated gp91(phox) reduction could be one of the mechanisms involved in atorvastatin's antioxidant effect.
Abstract: OBJECTIVES: Our goal was to explore whether antioxidant vitamin C infusion is able to affect the microcirculation perfusion in patients undergoing elective percutaneous coronary intervention for stable angina. BACKGROUND: Periprocedural myocardial injury in the setting of elective percutaneous coronary intervention is associated with increased risk of death, recurrent infarction, and revascularization at follow-up. Despite excellent epicardial blood flow, impaired microcirculatory reperfusion may persist and increases the risk of vascular recurrences. Post-percutaneous coronary intervention induced-oxidative stress is one of the potential mechanisms accounting for impaired perfusion. METHODS: Fifty-six patients were enrolled in a prospective, single-center, randomized study comparing 1 g vitamin C infusion (16.6 mg/min, over 1 h before percutaneous coronary intervention) versus placebo. RESULTS: At the baseline, Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade <2 was observed in 89% and in 86% of patients randomized to the placebo or vitamin C infusion group, respectively (p > 0.05). After percutaneous coronary intervention, these percentages decreased in the placebo group (32%) and in greater measure in the vitamin C group (4%, p < 0.01). Complete microcirculatory reperfusion (TIMI myocardial perfusion grade = 3) was achieved in 79% of the vitamin C-treated group compared with 39% of the placebo group (p < 0.01); 8-hydroxy-2-deoxyguanosine (p < 0.002) and 8-iso-prostaglandin F(2alpha) (p < 0.02) plasma levels significantly increased in the placebo group while they were significantly reduced in the vitamin C-treated group (p < 0.0001). TIMI myocardial perfusion grade changes from the baseline showed significant correlation with 8-hydroxy-2-deoxyguanosine (p < 0.006) or 8-iso-prostaglandin F(2alpha) (p < 0.01) plasma levels changes. CONCLUSIONS: In patients undergoing elective percutaneous coronary intervention, impaired microcirculatory reperfusion is improved by vitamin C infusion suggesting that oxidative stress is implicated in such a phenomenon.
Abstract: Objectives: The -765G>C variation (rs20417 SNP) in the promoter of cyclooxygenase-2 (COX-2) gene has been demonstrated to lower COX-2 enzyme activity in the vasculature, thus affecting atherosclerotic plaque growth and stability. Therefore, this genetic variant may be a candidate influencing the residual risk. Methods: In 285 coronary patients the incidence of major adverse cardiovascular events (MACEs), defined as a composite of cardiovascular deaths, non-fatal myocardial infarction and stroke, unstable angina and revascularization procedures, was monitored for a median of 7.8 years. The genotypes were obtained in 231 patients (81%) by PCR amplification and FAU I digestion. Results: 89 MACEs (38.5%) were recorded during the follow-up in genotyped patients. Their incidence was not different in patients with GC or CC when compared with those with GG genotype (46.2 vs. 35.5% respectively; p = 0.14). Kaplan-Meyer analysis did not demonstrate any influence of COX-2 genotypes on the event-free survival time (log-rank p = 0.55). After controlling for confounders, the -765G>C carrier status was not associated with significant variation in the risk of MACE or its individual components. Conclusions: These results suggest that the functional G-765C variant in the COX-2 gene is not a significant predictor of the recurrence of ischemic events in coronary patients.
Abstract: Background: No previous study has assessed the possible role of dipyridamole for treatment of no-reflow during acute myocardial infarction (AMI). Methods and Results: Forty-six consecutive patients (age 64 +/- 13 years, 37 men) with no reflow during primary percutaneous coronary intervention were randomized to initial treatment with either dipyridamole (0.56 mg/kg i.c.) or verapamil (1 mg i.c.). Patients with unsuccessful response to the first drug were then switched to the second one (from dipyridamole to verapamil and vice versa). Angiographic end-points were similar in the two groups: TIMI flow was 2.9 +/- 0.3 versus 2.8 +/- 0.4 (P = 0.28), corrected TIMI frame count (cTFC) 26.4 +/- 8.8 versus 31.6 +/- 11.4 (P = 0.14) and TIMI myocardial perfusion grade (TMPG) 2.1 +/- 1.2 versus 1.7 +/- 1.2 (P = 0.12) in dipydidamole and verapamil group, respectively. Optimal myocardial perfusion (TMPG-3) was achieved by 56% of patients with dipyridamole and 39% with verapamil (P = 0.38). In patients with persistent no-reflow administration of dipyridamole on top of verapamil resulted in a significant further improvement of cTFC (from 31.6 +/- 11.4 to 24.6 +/-5.7 P = 0.009) and of TMPG (from 1.7 +/- 1.2 to 2.6 +/- 0.7, P = 0.007). Conversely, verapamil did not induce a significant improvement in coronary flow (cTFC changed from 26.4 +/- 8.8 to 24.5 +/- 8.5, P = 0.28 and TMPG from 2.1 +/- 1.2 to 2.4 +/- 1.2, P = 0.13). There were no significant side effects induced by dipyridamole, while verapamil caused AV block in 9% of cases. Conclusions: Dipyridamole is a safe and effective first-line drug for treatment of no-reflow. Dipyridamole can also be successfully used in patients with incomplete response to verapamil. (c) 2010 Wiley-Liss, Inc.
Abstract: Summary Objectives: To reduce the increase of oxidative stress and the upregulation of CD40L during stenting procedure using ascorbic acid infusion. Background: CD40L upregulation occurring after coronary Percutaneous Coronary Intervention predicts vascular events but the underlying mechanism is still unclear. Methods: Fifty-six patients undergoing elective coronary stenting were randomly allocated to intravenous infusion of the antioxidant ascorbic acid or placebo. Platelet CD40L and plasma levels of soluble CD40L and of 8-hydroxy-2'-deoxyguanosine, a marker of oxidative stress, were measured before and after coronary stenting. In vitro study was also done to measure reactive oxidant species and CD40L expression in platelets exposed to anoxia-reoxygenation. Results: Placebo-treated patients showed a significant increase of platelet CD40L, soluble CD40L and 8-hydroxy-2'-deoxyguanosine compared to baseline values. Patients given ascorbic acid showed no change of soluble CD40L and platelet CD40L but a significant decrease of 8-hydroxy-2'-deoxyguanosine. After 60 and 120 min, soluble CD40L, platelet CD40L and 8-hydroxy-2'-deoxyguanosine were significantly lower in the ascorbic acid-treated group compared to the placebo-treated one. A significant correlation between platelet CD40L and soluble CD40L and between soluble CD40L and 8-hydroxy-2'-deoxyguanosine was observed. Platelets, in vitro exposed to anoxia-reoxygenation, had a burst of ROS and an upregulation of CD40L that were inhibited by ascorbic acid or apocynin, an inhibitor of NADPH oxidase. Conclusions: This study shows that in patients undergoing coronary stenting CD40L is upregulated with a mechanism which is likely mediated by oxidative stress.
Abstract: Statin interference has been suggested among the mechanisms of reduction of the antiplatelet effect of clopidogrel. We thus sought to assess the influence of rosuvastatin on clopidogrel antiplatelet action in high-risk (HR) cardiovascular patients. To set the level of platelet inhibition by combined antithrombotic treatments we retrospectively studied two populations of HR patients, one under aspirin alone, the other under aspirin plus rosuvastatin, before and after addition of clopidogrel. The effects of rosuvastatin compared with atorvastatin were then prospectively investigated in patients who underwent percutaneous coronary intervention (PCI), under clopidogrel and aspirin treatment. Light transmission platelet aggregation (LTA) was studied in response to adenosine diphosphate (ADP) (5 microM) or arachidonic acid (0.5 mM). The inhibitory effect of clopidogrel in reducing ADP-induced LTA was similar in the two HR groups of patients. No difference in ADP-induced platelet aggregation was observed in the two PCI groups of patients with either atorvastatin or rosuvastatin. In conclusion, rosuvastatin does not interfere with the antiplatelet effect of clopidogrel in patients with cardiovascular disease.
Abstract: BACKGROUND: The 64-slice multidetector-row computed tomography (MDCT) is an accurate noninvasive technique for assessing the degree of luminal narrowing in coronary arteries of patients with chronic ischemic disease. Aim of this study was to determine the value of MDCT in comparison to invasive coronary angiography (ICA) for detecting the presence and extent of coronary atherosclerotic plaques in a population of asymptomatic, hypertensive patients considered to be at high risk for cardiovascular events. METHODS: We studied 67 asymptomatic, hypertensive patients at high-risk (Euro Score >5%). All patients had negative or nondiagnostic findings at exercise stress testing and therefore underwent both MDCT and ICA. RESULTS: In the per-patient analysis, MDCT correctly identified 16/17 (94%) patients with significant coronary artery disease involving at least 1 vessel and 48/50 (96%) normal subjects. In the per-segment analysis, MDCT correctly detected 21/22 (95%) coronary segments with a stenosis >or=50% and 856/868 (98%) normal segments, with a high negative predictivity of normal scans (100%). There was a good concordance between MDCT and ICA, with a high Pearson correlation coefficient between the coronary narrowings with the two techniques (r=0.84, p<0.01). Mean coronary calcium score was higher for the 17 patients with significant coronary artery disease on ICA than in the 50 patients without (422+/-223 HU vs 72+/-21 HU p<0.001). The ROC curves identified 160 as the best calcium volumetric score cut-off value able to identify >or=1 significant coronary stenosis with sensitivity 88% and specificity 85%. CONCLUSIONS: MDCT is an excellent noninvasive technique for early identification of significant coronary stenoses in high risk asymptomatic hypertensive patients and might provide unique information for the screening of this broad population.
Abstract: It remains unclear whether dual antiplatelet therapy >12 months might carry a better prognosis after percutaneous coronary intervention (PCI) with drug-eluting stents (DESs). To address the hypothesis that in the real world the risk of very late thrombosis after PCI with DESs can be decreased by an extended use of clopidogrel, we set up the Two-Year ClOpidOgrel Need (TYCOON) registry and prospectively investigated the impact on very late thrombosis of 12- versus 24-month dual antiplatelet regimens in an unselected population. The registry enrolled 897 consecutive patients who underwent PCI with stenting from January 1, 2003, to December 31, 2004, and had dual antiplatelet therapy. All patients had a 4-year clinical follow-up. In the 447 patients with DES implantation, the dual antiplatelet regimen after PCI was given for 12 months in the 173 patients treated in 2003 (12-month group) and for 24 months in the 274 patients treated in 2004 (24-month group). Comparison between groups did not reveal any significant difference in baseline clinical characteristics, angiographic and procedural features, and major adverse cardiac events. During follow-up, there were 5 cases of stent thrombosis after PCI in the 12-month DES group and 1 case in the 24-month DES group (p = 0.02). Specifically, there were 2 cases of subacute thrombosis (1 in each group), no case of late thrombosis, and 4 cases of very late thrombosis occurring at 13, 15, 17, and 23 months after DES implantation in the 12-month group only. In conclusion, a 2-year dual antiplatelet regimen with aspirin and clopidogrel can prevent the occurrence of very late stent thrombosis after PCI with DESs.
Abstract: BACKGROUND: Chest pain is frequently reported in Fabry disease (FD). However, its mechanism and clinical relevance are unclear. METHODS AND RESULTS: Basal troponin I level, exercise stress test, single-photon emission computed tomography imaging with (99m)Tc sestamibi, coronary angiography with thrombolysis in myocardial infarction (TIMI) frame count and left ventricular angiography and endomyocardial biopsy were obtained in 13 patients with FD with angina. Ratio of external to lumen diameter of intramural arteries (E/L ratio), myocyte diameter, and extent of fibrosis were morphometrically evaluated by using tissue sections. Controls for coronary angiography and histology were 25 patients with FD without angina and 20 mitral stenosis patients with normal left ventricular function. Troponin I level was elevated in 6 of the 13 patients. Exercise stress test showed evidence of myocardial ischemia, and single-photon emission computed tomography was positive for stress-induced perfusion defects in all patients with FD with angina. Epicardial coronaries were structurally normal but showed slow flow in all and were associated with aneurisms of posterior left ventricular wall in 3 cases. Histology showed remarkable lumen narrowing of most intramural arteries (mean E/L ratio=3.5+/-1.2; P<0.001 versus both control groups), because of hypertrophy and proliferation of smooth muscle and endothelial cells, both engulfed by glycosphingolipids. Replacement fibrosis exceeded that of both controls (P<0.001). Small vessel disease correlated with coronary slow flow and extent of fibrosis, but did not with patients' age, sex, and degree of left ventricular hypertrophy. CONCLUSIONS: patients with FD with angina have perfusion defects, slow coronary flow, and luminal narrowing of intramural arteries. Small vessel disease may contribute to symptomatic limitation and progressive myocardial dysfunction.
Abstract: OBJECTIVE: The common C242T polymorphism in the gene for the p22phox subunit of NADPH oxidase has been reported to be negatively associated with oxidative stress, but whether it confers prognostic information is not yet clear. METHODS AND RESULTS: The incidence of major adverse cardiovascular events (MACE) were determined in 237 patients with coronary stenosis during a median follow-up of 7.8 years. The p22phox genotypes were evaluated in 213 patients (89.9%) by polymerase chain reaction and RsaI. digestion. Plasma levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative stress, were also measured. In the univariate analysis, patients with CT/TT genotypes showed reduced recurrence of cardiovascular deaths, nonfatal MI, and revascularization procedures compared with homozygous carriers of the C allele. After controlling for confounders, a significantly lower risk of new revascularization procedures (HR=0.31, 95% CI 0.12 to 0.70; P=0.014) remained associated with the T allele. The Kaplan-Meier analysis showed a longer survival free from fatal and nonfatal MI in carriers of T allele (P<0.001). The presence of the 242T allele was associated with significantly reduced plasma concentrations of 8-OHdG. CONCLUSIONS: The 242T allele was a predictor of lower risk of recurrence of cardiovascular events in high-risk patients and was associated with reduced systemic oxidative stress.
Abstract: The identification of factors contributing to residual cardiovascular risk is important to improve the management of patients with established coronary artery disease (CAD). This study was conducted to assess the predictive value of atherogenic dyslipidemia (defined as high triglycerides and low high-density lipoprotein [HDL] cholesterol) for long-term outcomes in patients with CAD. In 284 patients (238 men, 46 women; mean age at baseline 59.2 +/- 8.9 years) with coronary stenosis (>50% in > or =1 vessel), the presence of atherogenic dyslipidemia was prospectively associated with the incidence of major adverse cardiovascular events (MACEs) during a median follow-up of 7.8 years. MACEs were defined as cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, the recurrence of angina, and revascularization procedures. MACEs were observed in 111 (39.1%) patients with CAD. MACEs occurred more frequently in patients with atherogenic dyslipidemia (50.9%) than in those with isolated low HDL cholesterol or high triglycerides (33.0%) or with normal HDL cholesterol and triglyceride concentrations (29.2%) (p <0.01 for trend). Kaplan-Meier survival analysis showed a decrease in event-free survival in patients with compared with those without atherogenic dyslipidemia (log-rank p = 0.006). Patients with atherogenic dyslipidemia presented with increased plasma concentrations of remnants, denser low-density lipoprotein, more atherogenic HDL particles, and insulin-resistant status. After adjustment for potential confounding variables, the magnitude of increased risk associated with atherogenic dyslipidemia was 1.58 (95% confidence interval 1.12 to 2.21, p = 0.008). In conclusion, these data provide evidence that atherogenic dyslipidemia is an independent predictor of cardiovascular risk in patients with CAD, even stronger than isolated high triglycerides or low HDL cholesterol.
Abstract: Aims: The long-term outcome of extended dual antiplatelet therapy after percutaneous coronary intervention (PCI) is unexplored. The purpose of the study was to evaluate the 2 year safety and efficacy of continuous dual antiplatelet treatment in patients undergoing primary PCI with paclitaxel-eluting stent (PES) for acute ST segment elevation myocardial infarction (STEMI).Methods and results: A series of 145 consecutive patients with STEMI underwent primary PCI with PES. All patients received intracoronary high dose bolus and 24 hours i.v. infusion of tirofiban and were then treated with dual anti-aggregation up to 2 years. The incidence of major adverse cardiac events (MACE) was evaluated at 1 month, 1 year, and 2 years during the follow-up period. Overall, the rate of cumulative MACE detected at follow-up was 2.7%, with a 1.4% incidence of mortality and a 0.7% need for target vessel revascularisation. No major bleeding occurred during follow-up (95% C.I. 0-2.6%). Safety analysis revealed that minor bleeding occurred in 5 patients (3.4%) at the time of PCI, and that thrombocytopenia developed in 3 patients (2.1%) with the extended clopidogrel course. During the 2 year follow-up, in-stent thrombosis was seen in only 1 patient who stopped drug treatment against medical advice, but did not occur in patients who remained on dual antiplatelet therapy.Conclusions: This study shows in a 'real world' scenario that sustained dual antiplatelet therapy following primary PCI with PES in patients with STEMI is associated with very good 2 year clinical results.
Abstract: Being usually asymptomatic, anomalous coronary arteries (ACAs) are discovered in adulthood using invasive coronary angiography (CA) performed for suspected coronary artery disease. However, if only based on CA, the correct diagnosis is not easily made. We report on the importance of integrated data obtained by using multidetector computed tomography, and perfusional myocardial scintigraphy as alternative non-invasive imaging techniques in evaluating the exact course and the functional importance of usually considered "benign" ACAs in three symptomatic subjects, and of the development of official recommendations for the practitioners in the management of such patients.
Abstract: The tako-tsubo syndrome is a transient cardiomyopathy of unknown origin, which mimics acute ST-elevation myocardial infarction in the absence of obstructive epicardial coronary artery disease. This novel syndrome is characterized by chest pain, ST-segment changes, minimal enzymatic release, and balloon-like asynergy of the apical region. We report a case of tako-tsubo syndrome associated with acute cytomegalovirus infection and discuss the possible role of a viral aetiology in the onset of this syndrome.
Abstract: OBJECTIVE: We investigated myocardial perfusion in acute patients with slow coronary flow (SCF) at angiography. Whether impaired myocardial perfusion occurs in acute patients with SCF is unknown. METHODS: We enrolled 28 consecutive patients with SCF in the epicardial coronary arteries with no evidence of significant stenosis. SCF affected a single coronary artery in 14 patients (group A) and all three coronary vessels in 14 others (group B). Coronary angiography was repeated after dipyridamole infusion and single photon emission computed tomography was performed using dipyridamole as the stress agent. The Thrombolysis in Myocardial Infarction frame count was measured in SCF vessels at baseline and after dipyridamole infusion. RESULTS: Mean Thrombolysis in Myocardial Infarction frame count significantly decreased after dipyridamole in both groups. At baseline, mean values of the single photon emission computed tomography score were 31.5 +/- 1.6 and 25.1 +/- 2.1 in groups A and B, respectively. After dipyridamole, they increased from 31.5 +/- 1.6 to 37.8 +/- 1.4 (P < 0.001) in group A, whereas a further decrease to 15.0 +/- 1.2 (P < 0.005) was observed in group B. CONCLUSIONS: An opposite behavior of myocardial perfusion was observed after dipyridamole infusion: a normal response in patients with SCF affecting one single coronary artery versus an ischemic-like response in those with CSF affecting all three coronary arteries.
Abstract: BACKGROUND: Coronary artery disease (CAD) is the most common cause of hospitalization and mortality in many industrialized countries. We analysed the diagnostic accuracy of multi-detector row spiral computed tomography (MDCT) in determining mid- to high-grade coronary artery stenoses (> 50%). METHODS: Sixty-nine patients with suspected CAD were referred to MDCT coronary angiography. Patients with a heart rate above 60 bpm received 20-40 mg propranol before the scan. The left main (LM), the left anterior descending artery (LAD), the first diagonal branch (D1), the right coronary artery (RCA) and the proximal tract of the circumflex artery (LCX) were independently evaluated by two blinded observers and screened for > 50% stenoses. The mean values of MDCT coronary narrowings assessed by two observers were compared to quantitative coronary angiography. RESULTS: MDCT correctly detected 95 of 123 coronary lesions (sensitivity 77.2%) and absence of stenoses was correctly identified in 388 of 426 segments (specificity 91%). The sensitivity for the LM, LAD, RCA and the proximal tract of LCX was 100%, 86.5%, 69.8% and 80% respectively. Classification of patients as having 1-vessel, 2-vessels, 3-vessels or left main disease was accurate in 75.4% (46/61) of patients. CONCLUSIONS: MDCT technology, combined with heart rate control, allows reliable noninvasive detection of hemodynamically significant CAD.
Abstract: PURPOSE: To detect coronary artery stenoses, we compare breath-hold magnetic resonance coronary angiography (MRCA) to conventional coronary angiography (CA). MATERIALS AND METHODS: Sixty-five patients with suspected coronary artery disease underwent MRCA and CA within one week. MRCA examination was performed by using the two-dimensional (2D) breath-hold technique with a fast spoil gradient-echo sequence/spiral. Each imaging sequence was obtained within one breath-hold in expiration (14 seconds of apnoea). The assessment of coronary artery stenoses on magnetic resonance (MR) angiograms was independently performed by two blinded readers and compared to conventional CA images. RESULTS: Three hundred and ninety segments were evaluated by the two imaging techniques. MRCA correctly detected 76 of 88 (86%) stenoses, and recognized 242 of 302 (80%) not affected segments. The Pearson correlation coefficient between MRCA and CA in assessing coronary narrowings was very high: r = 0.85. Despite this the mean difference was 4.5 with a standard error of estimate of 0.21, indicating that MRCA slightly overestimates the degree of stenoses. CONCLUSIONS: Our study showed that 2D breath-hold MRCA is an accurate technique in displaying and quantifying the most significant stenoses in the proximal and middle segments of the coronary arteries.
Abstract: BACKGROUND: The hypothesis that in normotensive offspring of hypertensive parents exercise training could influence the systemic release of endothelin (ET)-1 during a provocative testing protocol was tested. METHODS: The provocative handgrip test was performed in four groups of healthy young age-matched males: offspring of hypertensive parents following a regular swimming exercise regimen (group A, n = 14); offspring of hypertensive parents and leading a sedentary lifestyle (group B, n = 11); normal volunteers with no family history of hypertension: sedentary (group C, n = 10), and following a regular swimming regimen (group D, n = 10). The plasma ET-1 was measured at baseline, after 4 min of handgrip exercise at 50% maximal capacity and following 2 (R2) and 10 (R10) min of recovery from handgrip. RESULTS: ET-1 plasma levels, within the normal range in all groups at baseline (group A 0.94 +/- 0.32 pg/ml, group B 0.84 +/- 0.26 pg/ml, group C 0.78 +/- 0.35 pg/ml, group D 0.85 +/- 0.26, p = NS) showed a progressive and significant increase in group B during and after handgrip exercise (peak handgrip 1.08 +/- 0.5 pg/ml, p = NS; R2 1.35 +/- 0.36 pg/ml, p < 0.05; R10 2.76 +/- 0.75 pg/ml, p < 0.01). Significant differences were found at R2 and R10 when the ET-1 levels measured in group B were compared to those observed in group A, group C and group D. Multivariate analysis demonstrated that the serum levels of ET-1 significantly contributed to predict handgrip-induced changes when the diastolic blood pressure was the dependent variable. CONCLUSIONS: Routine aerobic exercise appeared to counteract the handgrip-induced abnormal release of plasma ET-1 and may favorably affect the preclinical endothelial alterations seen in healthy offspring of hypertensive parents.
Abstract: Relying on the synergistic action on contractility of enoximone and dobutamine when concomitantly infused, 25 patients with their first acute Q-wave anterior myocardial infarctions underwent conventional low-dose dobutamine echocardiography (LDE) and enoximone very-LDE to assess myocardial viability in severely dysfunctioning areas. Images were recorded at peak of pharmacodynamic effect of drugs and 4 months after revascularization. At peak-dose stage of LDE and enoximone very-LDE the regional infarct zone wall-motion score significantly decreased from the basal value of 25.6 +/- 2.9 to 16 +/- 6.0 (P <.001) and to 14.5 +/- 5.2 (P <.001), respectively. A high correlation was found by comparing the wall-motion score of each patient calculated at peak effect of combined drug administration with follow-up values (r(s) = 0.9). Enoximone very-LDE has proven to be a new test useful to evaluate viability in asynergic segments especially when the results of conventional tests are questionable.
Abstract: BACKGROUND: The present study evaluated the role of the PON1 L55M polymorphism independently and in conjunction with the Q192R polymorphism on the risk of coronary atherosclerosis in an Italian population. MATERIALS AND METHODS: Three hundred and ninety-one subjects with significant coronary stenosis (> 50%) (coronary artery disease-positive; CAD+), 196 subjects with normal coronary arteries (< 10% stenosis) (CAD-) and 178 healthy controls were screened using a combination of polymerase chain reaction and restriction enzyme digestion. RESULTS: In the pooled population, the frequencies of L and M alleles were 0.63 and 0.37, respectively; the most common haplotypes were QQ/LM (24.2%) and QR/LL (21.8%) and a strong linkage disequilibrium between L/55 and R/192 alleles was observed (D' = -0.91; P < 0.0001). CAD+ subjects did not show any significant differences in the distribution of PON1-55 genotypes as compared to CAD- subjects and population controls (chi2 = 1.5, P = 0.8). After controlling for other risk factors, the low-concentration M allele was not associated with a significant change of CAD risk (OR 1.02; 95% CI 0.80-1.29; P = 0.87). Moreover, the L55M polymorphism did not show any interaction with other risk factors such as smoking, diabetes, hypertension, low levels of high-density lipoprotein (HDL) or high ratios of low-density to high-density lipoproteins. The combination of L55M with the Q192R polymorphism did not show any effect on CAD risk. However, a marginal decrease in myocardial infarction risk was detected when QQ/MM carriers (OR 0.51; 95% CI 0.26-0.99; P = 0.048), but not LL/RR carriers, were compared with subjects not homozygous for an L or R allele. CONCLUSIONS: These findings did not indicate a major effect of the PON1 L55M polymorphism, either alone or in combination with the Q192R polymorphism, on CAD risk. Additional studies are needed for a better evaluation of the role of the 55/192 PON1 genotypes in combination on myocardial infarction risk.
Abstract: The present study evaluated the role of the common lipoprotein lipase (LPL) mutations on the risk of dyslipidemia and coronary atherosclerosis in an Italian population. Cohorts of 632 patients undergoing coronary angiography, as well as 191 healthy controls, were screened by a combination of PCR and restriction enzyme digestion. In the pooled population, the frequencies of LPL D9N and N291S were 4.1%, with no homozygous carriers, whereas that of LPL S447X was 21% with 19.6% heterozygous and 1.4% homozygous carriers. Compared to non-carriers, LPL N291S carriers showed higher plasma triglycerides (TG) (p < 0.03) and increased risk of high TG phenotype (odds ratio [OR] 2.49, 95% Cl 1.06-5.81; p < 0.03). When this LPL mutation was associated with high body mass index (BMI) ( > 25 Kg/m2) or fasting, plasma insulin (> 10.6 mU ml(-1)) significantly reduced HDL-C levels were also observed. Carriers of the S447X mutation presented with higher HDL-C concentrations (p < 0.05) as compared to non-carriers; they also showed a significantly reduced risk of high TG/low HDL-C dyslipidemia (OR 0.34, 95%, Cl 0.12-0.99; p < 0.05). The favourable effect of the LPL S447X variant was even more pronounced in lean subjects and in those with low insulin levels. No significant influence on plasma lipids by the LPL D9N was observed. None of LPL variants was a significant predictor of angiographically assessed coronary atherosclerosis. At most, the risk was borderline, increased in N291S carriers and possibly decreased in S447X carriers.
Abstract: Dobutamine and enoximone stimulate independently inotropic reserve by increasing intracellular cyclic adenosine monophosphate. The potential of enoximone (0.75 mg/kg body weight over 10 minutes) followed by very low dose (2.5 microg/kg/min) dobutamine echocardiography to predict recovery of ventricular function in akinetic and dyskinetic postinfarcted areas was studied. We enrolled 22 patients with previous Q-wave myocardial infarction and regional wall motion abnormalities related to left anterior descending arterial disease, left ventricular ejection fraction <40%, and all scheduled for myocardial revascularization. A 10 microg/kg/min dobutamine test was performed 48 hours before the study protocol. Test images obtained at peak of pharmacodynamic effects were compared with those obtained at 4 months after myocardial revascularization. We used a 16-segment ventricular model and a 5-grade scoring system. Resting regional myocardial dysfunction graded > or =2 was present in 267 of 352 segments evaluated. Contractile reserve (decrease in resting wall motion score > or =2 grades) at peak effect of enoximone infusion was present in 34 of 112 severely hypokinetic, 42 of 117 akinetic, and 14 of 38 dyskinetic segments. The inotropic reserve evaluated after very low dose dobutamine was observed in 34 of 112 severely hypokinetic, 49 of 117 akinetic, and 20 of 38 dyskinetic segments. After revascularization, recovery of function was observed in 31 of 112 severely hypokinetic, 49 of 117 akinetic, and 21 of 38 dyskinetic segments. Overall, there was a significant correlation between absolute score changes of segments which were abnormal at baseline (n = 267) to enoximone peak effects (r = 0.49, p <0.001) to predict absolute changes after revascularization; after dobutamine there was progress toward identity (r = 0.62, p <0.001) and the difference was significant among correlation slopes of dobutamine alone, enoximone alone, and enoximone plus very low dose dobutamine echocardiograophy (0.45+/-0.04, 0.51+/-0.04, and 0.63+/-0.04, respectively, F = 5.25, p = 0.005). Therefore, enoximone followed by very low dose dobutamine may assess myocardial viability of postinfarcted akinetic and dyskinetic areas. This test may be useful when evaluating patients with more severe cardiac failure and/or life-threatening arrhythmias.
Abstract: OBJECTIVES: We tested the hypothesis that an abnormal response of plasma endothelin-1 (ET-1) is elicited by handgrip exercise (HG) in young normotensive offspring of hypertensive parents. BACKGROUND: It has been hypothesized that ET-1 is involved in blood pressure control and plays a pathophysiologic role in the development of clinical hypertension. METHODS: Two groups of healthy male subjects, 11 with hypertensive parents (group A) and 10 without a family history of hypertension (group B), underwent 4 min of HG at 50% maximal capacity. Heart rate and blood pressure and plasma levels of ET-1, epinephrine and norepinephrine were measured at baseline, peak HG, and after 2 (R2) and 10 (R10) min of recovery. RESULTS: Group A had higher norepinephrine levels than group B throughout the test (baseline 181+/-32 [SEM] vs. 96+/-12 pg/ml, p < 0.05; peak HG 467+/-45 vs. 158+/-12 pg/ml, p < 0.000001; R2 293+/-46 vs. 134+/-8 pg/ml, p < 0.01; RO1 214+/-27 vs. 129+/-10 pg/ml, p < 0.0005); no significant difference in epinephrine levels was detected. Compared with group B subjects, group A had higher baseline ET-1 levels (1.07+/-0.14 vs. 0.59+/-0.11 pg/ml, p < 0.02), which increased to a greater extent at peak HG (1.88+/-0.31 vs. 0.76+/-0.09 pg/ml, p < 0.005) and R2 (2.46+/-0.57 vs. 1.31+/-0.23 pg/ml, p < 0.05) and remained elevated at R10 (3.16+/-0.78 vs. 0.52+/-0.09 pg/ml, p < 0.002). Multivariate analysis demonstrated that only a family history of hypertension (chi-square=7.59, p=0.0059) and ET-1 changes during HG (chi-square=4.23, p=0.0398) were predictive of blood pressure response to HG and that epinephrine and norepinephrine were not. CONCLUSIONS: The response to HG in offspring of hypertensive parents produced increased ET-1 plasma levels and resulted in a sustained ET-1 release into the bloodstream during recovery compared with offspring of normotensive parents. This may be an important marker for future clinical hypertension.
Abstract: BACKGROUND: Trimetazidine is an antiischemic drug protecting the myocardium from ischemic damage through the preservation of mitochondrial oxidative metabolism, without any hemodynamic effect. 99mTc-sestamibi is accumulated by myocytes according to mitochondrial function. As mitochondrial metabolism is thought to be present in hibernating myocardium, the aim of the study was to investigate trimetazidine effects on infarcted and eventually hibernating myocardial areas by means of 99mTc-sestamibi perfusional scintigraphy, comparing them to postoperative recovery of wall motion. METHODS AND RESULTS: Twelve patients with previous myocardial infarction underwent 2 perfusion imaging tomographic studies at rest with 99mTc-sestamibi, receiving placebo or trimetazidine (60 mg orally), and subsequently underwent revascularization procedures. An echocardiographic study was carried out before and >3 months after revascularization. At polar map analysis of placebo scan, infarcted vascular territories (wall motion score index: 2.65 +/- 0.31) showed 73.7% +/- 10.4% of the territory with activity <2.5 SD from the mean of normals, for a severity (expressed as the sum of the standard deviations below average normal values in all abnormal pixels) of 833.8 +/- 345.7. Polar map analysis of the trimetazidine scan showed tracer uptake increased significantly in 11 of them, by 8.2% +/- 3.0% (p < 0.001) and by 180.3 +/- 111.0 SD (p < 0.001), respectively. Postoperative wall motion score index improved significantly in 9 of these territories (-0.9 +/- 0.4, p < 0.001). CONCLUSIONS: Trimetazidine-associated increase in 99mTc-sestamibi uptake in infarcted but viable myocardial areas is probably related to an improvement in mitochondrial oxidative metabolism that is essential to 99mTc-sestamibi retention. Additionally, coupling trimetazidine administration to 99mTc-sestamibi perfusional scintigraphy may represent a means of detecting viable myocardium.
Abstract: Corrected transposition of the great arteries is a rare congenital heart disease, affecting 1% of children with cardiac malformation. Patients with transposition of the great arteries and without associated cardiovascular anomalies are very infrequent and may remain undiagnosed until adult life, because they usually are asymptomatic until the fourth or fifth decades. At this time, most symptoms occur in close connection with deterioration in systemic (right) ventricle performance and with an increase in left atrial pressure. In this report, we describe two new adult cases of isolated, corrected transposition of the great arteries, offering several considerations on their clinical profile and therapeutic assessment.
Abstract: To assess the comparative effects of benazepril and nitrendipine monotherapies on left ventricular mass index (LVMI) in hypertensive patients with echocardiographically determined left ventricular hypertrophy, patients with diastolic blood pressure (BP) > or = 100 mm Hg were randomized to benazepril, 10 mg, or nitrendipine, 20 mg, both given once or twice daily. After 4 weeks, only the responders (diastolic BP <90 mm Hg) entered a 5-month maintenance period. At baseline, and after 3 and 6 months, LVMI was blindly estimated by means of magnetic resonance imaging (MRI) and, for comparison, by means of echocardiography. Of the 50 randomized patients, three were excluded from the study as nonresponders after 4 weeks; moreover, two patients taking benazepril and one taking nitrendipine discontinued the treatment after 2 months for adverse effects. Both monotherapies reduced systolic and diastolic BP to a similar extent. After 3 months, MRI-estimated LVMI decreased by 21.5 g/m2 in the benazepril and 8.8 g/m2 in the nitrendipine group, with an adjusted mean difference between the two groups of 11.1 g/m2 (95% CI, 7.3-14.8 g/m2; p = 0.0001). After 6 months, it decreased by 23.6 g/m2 and 10.0 g/m2, respectively, with an adjusted mean difference of 11.3 g/m2 (95% CI, 7.5-15.5; p = 0.0001) in favor of benazepril. In conclusion, despite a similar antihypertensive effect, benazepril led to a greater reduction in MRI-measured LVMI than did nitrendipine (-16.2% vs. -7.2%) in hypertensive patients with left ventricular hypertrophy.
Abstract: In order to predict tissue viability in infarcted myocardial areas, changes induced by nitroglycerine infusion on Sestamibi myocardial uptake were evaluated in 37 patients with previously confirmed myocardial infarction undergoing coronary artery bypass grafting, and compared with echocardiographic and perfusional changes occurring after the operation. The improvement of Sestamibi uptake after nitroglycerine correctly classified 24/26 (92%) patients showing postoperative improvement of wall motion in the infarcted area, whereas 24/31 (77%) patients with nitroglycerine-induced increase in Sestamibi uptake had improved wall motion after operation. The presence of collateral flow to the infarcted area was associated with a significantly (P < 0.01) higher increase in Sestamibi uptake both during nitroglycerine infusion and postoperatively. An increase in wall motion score after operation was associated with a significantly higher (P < 0.05) increase in Sestamibi uptake score during nitroglycerine infusion. Thus, the results of this study suggest that Sestamibi perfusional myocardial scintigraphy during nitroglycerine infusion is capable of assessing viable but chronically hypoperfused myocardium and predicting postoperative wall motion and perfusional improvement, to yield the best results in patients with evidence of collateral circulation that supplies the infarcted area.
Abstract: This study demonstrated an immediate and short-lasting endothelin-1 release in the circulation of patients with severe chronic congestive heart failure during isometric handgrip exercise, but not in normal subjects. Our data suggest that endothelin-1 levels may increase transiently during daily physical activity, thus contributing to progressive deterioration of left ventricular function.
Abstract: Previous studies showed increased growth hormone (GH) plasma levels in patients with severe heart failure. It has been hypothesized that the activation of adenohypophysis determines the enhanced release of GH. The present study was designed to verify whether impaired hepatic function, due to biventricular cardiac failure and hepatic stasis, by reducing synthesis and release of insulin-like growth factor-1 (IGF-1), may affect the negative feedback mechanism of the IGF-1 on GH secretion. We studied 20 normotensive, non diabetic patients without primitive liver disease; 10 patients in NYHA functional class IV with clinical signs of biventricular cardiac impairment and hepatic stasis (Group A); 10 patients in NYHA functional class III with prevalent left ventricular dysfunction (Group B). Blood samples for radioimmunologic determination of GH, IGF-1, atrial natriuretic factor (ANF), proteins, albumin plasma levels and transaminase plasma levels measurements, were collected 24 hours before hemodynamic study. Group A patients had clinical and hemodynamic signs of hepatic stasis with impaired liver function (SGOT 68 +/- 5.5 U/l; SGPT 89 +/- 4.3 U/1; proteins 4.56 +/- 0.4 g/dl with albumin/globulin ratio < 1; albumin plasma levels 2.8 +/- 0.7 g/dl). The parameters were normal in Group B (SGOT 16 +/- 3.7 U/l;SGPT 13 +/- 1.9 U/l; proteins 7.5 +/- 0.7 g/dl with albumin/globulin ratio > or = 1.5;albumin plasma levels 4.2 +/- 1.2 g/dl). ANF values, over normal range in both groups, were significantly higher in Group A (157.9 +/- 43.9 vs 65.6 +/- 14.6 fmol/ml.p < 0.0001). In Group A GH values were increased (4.9 +/- 4.5 vs 0.12 +/- 0.04 ng/ml); on the contrary IGF-1 values were lower (187.9 +/- 98.2 vs 260.4 +/- 141.4 ng/ml, p < 0.01). The comparison between IGF-1 and albumin plasma levels showed a high correlation either in Group A (r = 0.88, p < 0.001;) or in Group B (r = 0.81, p < 0.001). Our findings allow to hypothesize that the reduced hepatic synthesis and release of IGF-1 may be responsible for the lack of trophic action of GH on cardiac myocytes in patients with biventricular heart failure and hepatic stasis.
Abstract: BACKGROUND: Nitroglycerin (NTG) is known to increase the blood supply to the myocardium, and would thus increase the delivery of a perfusional tracer such as sestamibi (MIBI) to the tissue. The latter, in turn, would take up and concentrate the tracer to a greater extent than in basal conditions only if energy-dependent mechanisms were still available-that is, only if the cells were still viable. METHODS: We evaluated the changes that intravenous administration of NTG induced on the uptake of MIBI by akinetic myocardial areas, using tomographic perfusional imaging in 23 patients with previously ascertained anterior myocardial infarction who were undergoing myocardial revascularization procedures. Changes in uptake were compared with echocardiographic and perfusional changes occurring after operation. RESULTS: The improvement of MIBI uptake after NTG correctly identified 12 of the 16 patients (75%) showing postoperative wall motion improvement; they comprised 12 of the 14 (86%) patients with NTG-induced increase in MIBI uptake who showed improved wall motion after operation. A close correlation (r = 0.88, P < 0.001) was found between the increase in myocardial MIBI uptake induced by NTG infusion and that induced by revascularization. The presence of collaterals to the akinetic area was associated with a significantly (P < 0.01) greater increase in MIBI uptake both during NTG infusion and after operation. CONCLUSIONS: The results of this study suggest that MIBI perfusional myocardial scintigraphy during infusion of NTG is capable of detecting viable but chronically hypoperfused myocardium, predicting postoperative wall motion and perfusional improvement, and reflecting the postoperative pattern of perfusion. The best results were achieved in patients with evidence of collateral circulation supplying the infarcted area.
Abstract: BACKGROUND: The hypothesis that in normal pituitary patients (pts) with heart failure the heart is a target-organ of the hypophysis has not be held in due consideration. Aim of the study was: 1) to determine Growth Hormone (GH) plasma levels in pts with various degree of heart failure; 2) to evaluate the relationship between GH, left ventricular mass and some haemodynamic and endocrine parameters of ventricular dysfunction. MATERIALS AND METHODS: Blood samples for determination of GH and Atrial Natriuretic Factor (ANF) were collected 24 hours before haemodynamic study. Plasma concentrations of GH and ANF were determined by radio-immuno-assay in 20 normotensive pts (age ranging 31 to 54) without mellitus diabetes in IV (10 pts) and III (10 pts) NYHA FC: Echocardiographic determination of left atrial diameter, end-diastolic and end-systolic left ventricular diameters, index of left ventricular mass (ILVM), were performed. All pts underwent right and left cardiac catheterization and coronary angiography. RESULTS: The pts in IV NYHA FC, Group A, had lower cardiac index (IC) (1.8 +/- 0.4 vs 2.9 +/- 0.1, p < 0.0001) and higher GH and ANF plasma levels than those in III NYHA FC, Group B (4.9 +/- 4.5 vs 0.12 +/- 0.04, p < 0.01; 157.9 +/- 43.9 vs 65.6 +/- 14.6, p < 0.0001). No significant difference was found by comparing in both groups ILVM (212.6 +/- 64.7 vs 192.9 +/- 71.9, NS). GH and ANF plasma levels were 4.1 +/- 5.0 and 113.8 +/- 59.6 in pts with ILVM > or = 200 g/mq and 0.9 +/- 2.7 and 109.7 +/- 57.3 in pts with ILVM < 200 g/mq (no significant statistical difference). We found an high correlation by comparing GH and ANF in group with ILVM > or = 200 g/mq (r = 0.82, p < 0.005) and in group with ILVM < 200 g/mq (r = 0.68, p < 0.05). CONCLUSIONS: Our study demonstrated: 1) increased GH plasma levels in pts with severe heart failure; 2) an high correlation between GH and ANF plasma levels in pts with ILVM > or = 200 g/mq.
Abstract: We studied the acute hemodynamic effects of nifedipine (N) on handgrip test (Hg) in 10 patients with aortic regurgitation in II NYHA functional class. In basal condition (B) we found a significant increase of mean aortic pressure (AoPmean) in all patients after Hg (101 +/- 9.72 versus 110.3 +/- 6.42 mmHg; p < 0.05). Hg did not induce significant changes of AoPmean after N. Hg increased left ventricular end-diastolic pressure (LVEDP) from 13.3 +/- 6.4 to 20.5 +/- 9.9 mmHg (p < 0.01) before N and from 9.7 +/- 3.2 to 12.8 +/- 5.5 mmHg after N (NS). LVEDP measured during Hg after N showed lower values than those measured before N (12.8 +/- 5.5 versus 20.5 +/- 9.9 mmHg; p < 0.01). Cardiac index (CI) increased by Hg in B (3.7 +/- 0.7 versus 4.0 +/- 1.1 L/min/m2; NS) and after N (4.5 +/- 0.7 versus 4.9 +/- 0.9 L/min/m2; NS). CI increased significantly after N at rest (3.7 +/- 0.7 versus 4.5 +/- 0.7 L/min/m2; p < 0.01) and during Hg (4.0 +/- 1.1 versus 4.9 +/- 0.9 L/min/m2; p < 0.01). The left ventricular stroke work index (LVSWI) decreased during Hg from 74.4 +/- 20.6 to 71.2 +/- 20.0 g.m/m2; NS. N caused an increase at rest to 81.4 +/- 22.5 g.m/m2; NS. LVSWI increased significantly during Hg to 83.5 +/- 26.2 g.m/m2; p < 0.05. Systemic arterial resistances (SAR) significantly decreased after N at rest (1,086.8 +/- 280.8 versus 843.5 +/- 133.1 dyne.s.cm-5; p < 0.01), but increased in B during Hg to 1,220.9 +/- 350.7 dyne.s.cm-5; p < 0.05. A significant reduction of SAR values was observed alter N during Hg (1,220.9 +/- 350.7 versus 838.9 +/- 139.9 dyne.s.cm-5; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Abstract: BACKGROUND: The recent introduction of percutaneous transvenous mitral valvuloplasty (PTMV) for the treatment of mitral stenosis (MS) has provided a unique human model for the study of short-term changes in ANF secretion before and after a reduction in left atrial pressure. This study was designed to investigate the effect of a short-term reduction in left atrial pressure and volume, as determined by echocardiographic study, on ANF and other neurohumoral factor plasma levels (renin and aldosterone). MATERIALS AND METHODS: 10 patients in III FC NYHA, with normal sinus rhythm and MS underwent PTMV. Hemodynamic parameters were measured immediately before and after (20-30 minutes) PTMV. Plasma levels of ANF, aldosterone and plasma renin activity (PRA) were obtained before (24 h) and after (2 h and 24 h) valvuloplasty; echocardiographic left atrial size before (24 h) and 24 h after PTMV. RESULTS: Immediately after PTMV mean left atrial (LA) pressure decreased from 22.3 +/- 6.8 mmHg to 10.0 +/- 2.4 mmHg (p < 0.01); mitral valve area (MVA) increased from 0.99 +/- 0.28 cm2 to 2.17 +/- 0.26 cm2 (p < 0.01). 24 hours after PTMV on echocardiography, LA systolic volume decreased from 59.5 +/- 16.9 cm3 to 42.3 +/- 8.3 cm3 (p < 0.01), LA diastolic volume from 82.6 +/- 15.8 cm3 to 66.5 +/- 12.6 cm3 (p < 0.01), and LA diameter from 48.1 +/- 7.5 mm to 39.2 +/- 4.4 mm (p < 0.01). ANF plasma levels before PTMV were 64.0 +/- 36.9 fmol/ml; 2 and 24 hours after PTMV they fell to 34.2 +/- 21.6 fmol/ml (p < 0.01) and to 20.3 +/- 21.0 fmol/ml (p < 0.01), respectively. PRA values were 15.7 +/- 13.2 ng/ml/h before PTMV; 2 and 24 hours after PTMV they increased to 17.5 +/- 23.2 ng/ml/h (NS) and to 22.3 +/- 16.8 ng/ml/h (p < 0.01). The aldosterone plasma levels were 43.2 +/- 27.9 ng/dl before PTMV and 47.3 +/- 35.8 ng/dl (NS) and 45.3 +/- 28.0 ng/dl (NS) 2 and 24 hours after PTMV. CONCLUSIONS: These results indicate that LA "de-stretching" due to the MVA increase and LA pressure decrease, leads to an abrupt reduction of ANF secretion. According to other studies, PRA increases immediately after PTMV, with a further increase 24 hours after PTMV.
Abstract: Atherosclerosis is the disease with the most important social impact in terms of cost and human life. Its study in the prevention and cure of its consequences needs integration using many imaging modalities, and magnetic resonance presents advantages due to its particular characteristics. The Authors make an overview of its indications and potential applications in the assessment of atherosclerotic disease. In vitro studies have demonstrated that it is possible to evaluate the normal and abnormal components of vessel walls by means of magnetic resonance imaging (MRI) as well as fatty deposition and intraplaque hemorrhage. On the other hand, in the in vivo studies, despite the impossibility to make a too fine structural analysis of the vessel wall, MRI allows to easily discriminate between blood flow and parietal wall. This is of great importance in the study concerning arterial aneurysms, that represent a consequence of atherosclerotic disease. Information as the presence, the site, the extension, the collateral vessel involvement and, finally, the presence or absence of dissection are all obtainable by using MRI. In the early 1990's magnetic resonance angiography (MRA) was developed and is now used in clinical practice. By means of this new application of MRI there is the possibility of increasing the non invasive screening of atherosclerosis especially in some body districts. The evaluation of the plaque obtainable by the combined use of MRA and ultrasound studies allows to decrease the employment of traditional and digital angiography. If, as studies predict, we will able to obtain coronary angiograms in the near future, there will be a further increase in the non invasive evaluation and in the prevention of atherosclerotic disease.
Abstract: The purpose of the study was to evaluate the value of magnetic resonance imaging as compared with two-dimensional echocardiography for a reliable assessment of the degree and distribution of apical hypertrophy in hypertrophic cardiomyopathy (HCM). The study includes 10 HCM patients (8 males and 2 females, mean age: 42 +/- 7 years). Two-dimensional echocardiography was not definitive in assessing the abnormal thickening of the apical myocardium in two patients. Two other patients had inadequate echocardiographic visualization of the lower left ventricle due to technical reasons. At magnetic resonance imaging, 3 patients showed localized hypertrophy at the left ventricular apex only. Three other patients had evidence of hypertrophy at the apex as well as at the left ventricular free wall. In four patients, the hypertrophy was detected at either the apex or the lower interventricular septum. It is concluded that magnetic resonance imaging might provide an accurate assessment of myocardial hypertrophy in HCM patients. This technique appears to be of major value in those with wall thickening localized to (or predominant in) the apical portion of the ventricle.
Abstract: Magnetic resonance imaging (MRI) was used to assess left ventricular mass (LVM) in 20 mild to moderate essential hypertensive patients with left ventricular hypertrophy (LVH) (LVM > 120 g/m2), treated with captopril alone or combined with hydrochlorothiazide. MRI examination was performed at the beginning (T0) and after 3 months (T3) of active treatment, by using a Philips Gyroscan S15 superconducting system, operating at 1.5 Tesla. We used a multislice-multiphase spin-echo sequence on the short-axis and transverse plane (TE = 30 ms; TR = 80-90% RR). End-diastolic thickness of interventricular septum (IVST) and lateral wall (LWT) were measured. LVM was calculated according to Simpson's rule. The results were: IVST 12.2 mm +/- 0.7 vs 10.9 mm +/- 0.5 (p < 0.001); LWT 11.5 mm +/- 0.9 vs 10.5 mm +/- 0.9 (p < 0.001); LVM 160 (g/m2) +/- 5.5 vs 138.4 g/m2 +/- 6 (p < 0.001), at T0 and T3, respectively. Our study demonstrates a significant regression of LVH in hypertensive patients after 3 months of treatment with captopril and a high accuracy of MRI as a noninvasive technique of measuring the LVM reduction.
Abstract: To assess the validity of gated magnetic resonance imaging (MRI) in determining left ventricular (LV) ejection fraction (EF), MRI (Spin Echo, multislice-multiphase technique on the short-axis plane) was compared with equilibrium radionuclide ventriculography in 32 patients with idiopathic dilated cardiomyopathy. All patients underwent MRI and radionuclide ventriculography, performed consecutively on the same day (mean time interval between the 2 examinations: 40 minutes). Comparison with LVEF showed a high correlation (y = 0.79 X +3.51, r = 0.91; p less than 0.001). Mean difference between radionuclide ventriculography and MRI data was 1.7, with the 95% confidence interval 0.71 to 2.68: MRI slightly underestimated LVEF. MRI interobserver and intrapatient variability (assessed in 15 of 32 patients) showed a high correlation (r = 0.91, r = 0.98). In conclusion, data suggest that MRI, using the short-axis approach and the multislice-multiphase technique, is an accurate, noninvasive, highly reproducible method of evaluating LVEF in patients with idiopathic dilated cardiomyopathy.
Abstract: The occurrence of concomitant first and second degree sinoatrial block due to chronic amiodarone treatment in 1 patient with moderate mitral valve stenosis is described. Discontinuation of amiodarone resulted in the disappearance of such a sinoatrial conduction disturbance.
