Obesity, estrone, and coronary artery disease in postmenopausal women.

OBJECTIVES: The link between obesity and endogenous estrogen with coronary artery disease (CAD) in postmenopausal women is uncertain. In this prospective study we analyzed the association of body mass index (BMI) and blood levels of estrone in postmenopausal women with known CAD or with a high risk factor score for CAD. METHODS: Participants were 251 female clinic patients aged 50-90 years who were postmenopausal and not using estrogen therapy. Clinical and behavioral characteristics and fasting blood for estrone and heart disease risk factors were collected at baseline, and again at 1 and 2 years. Women were grouped according to their BMI (kg/m2) as normal (18.5< or =BMI<25), overweight (25< or =BMI<30) or obese (BMI > or =30), and by low and high estrone levels (<15 and > or =15pg/mL, respectively). Fatal and nonfatal events were recorded for 2 years after baseline. RESULTS: Women with a low estrone level were older, thinner, and had less hypertension, diabetes, and lower triglyceride and glucose levels. BMI was positively associated with estrone levels, hypertension, and diabetes and inversely associated with HDL cholesterol. There were 14 deaths, 8 attributed to CAD. The Kaplan-Meier survival curve showed a nonsignificant trend (p=0.074) of greater all cause mortality in women with low estrone levels (<15mL). In this model, adjusted for BMI, age [OR=1.08; p=0.03], C-reactive protein [OR=1.24; p=0.024] and hypertension [OR=6.22; p=0.003] were independent predictors of all cause mortality. CONCLUSIONS: Postmenopausal women with low estrone levels (<15pg/mL) had a trend for increased mortality over the next 2 years. Larger, longer studies are needed.

Exercise stress testing before and after successful multivessel percutaneous transluminal coronary angioplasty.

Controversy exists regarding the diagnostic accuracy, optimal technique, and timing of exercise testing after percutaneous coronary intervention. The objectives of the present study were to analyze variables and the power of exercise testing to predict restenosis or a new lesion, 6 months after the procedure. Eight-four coronary multi-artery diseased patients with preserved ventricular function were studied (66 males, mean age of all patients: 59 +/- 10 years). All underwent coronary angiography and exercise testing with the Bruce protocol, before and 6 months after percutaneous coronary intervention. The following parameters were measured: heart rate, blood pressure, rate-pressure product (heart rate x systolic blood pressure), presence of angina, maximal ST-segment depression, and exercise duration. On average, 2.33 lesions/patient were treated and restenosis or progression of disease occurred in 46 (55%) patients. Significant increases in systolic blood pressure (P = 0.022), rate-pressure product (P = 0.045) and exercise duration (P = 0.003) were detected after the procedure. Twenty-seven (32%) patients presented angina during the exercise test before the procedure and 16 (19%) after the procedure. The exercise test for the detection of restenosis or new lesion presented 61% sensitivity, 63% specificity, 62% accuracy, and 67 and 57% positive and negative predictive values, respectively. In patients without restenosis, the exercise duration after percutaneous coronary intervention was significantly longer (460 +/- 154 vs 381 +/- 145 s, P = 0.008). Only the exercise duration permitted us to identify patients with and without restenosis or a new lesion.

Bioeffects of albumin-encapsulated microbubbles and real-time myocardial contrast echocardiography in an experimental canine model.

Myocardial contrast echocardiography has been used for assessing myocardial perfusion. Some concerns regarding its safety still remain, mainly regarding the induction of microvascular alterations. We sought to determine the bioeffects of microbubbles and real-time myocardial contrast echocardiography (RTMCE) in a closed-chest canine model. Eighteen mongrel dogs were randomly assigned to two groups. Nine were submitted to continuous intravenous infusion of perfluorocarbon-exposed sonicated dextrose albumin (PESDA) plus continuous imaging using power pulse inversion RTMCE for 180 min, associated with manually deflagrated high-mechanical index impulses. The control group consisted of 3 dogs submitted to continuous imaging using RTMCE without PESDA, 3 dogs received PESDA alone, and 3 dogs were sham-operated. Hemodynamics and cardiac rhythm were monitored continuously. Histological analysis was performed on cardiac and pulmonary tissues. No hemodynamic changes or cardiac arrhythmias were observed in any group. Normal left ventricular ejection fraction and myocardial perfusion were maintained throughout the protocol. Frequency of mild and focal microhemorrhage areas in myocardial and pulmonary tissue was similar in PESDA plus RTMCE and control groups. The percentages of positive microscopical fields in the myocardium were 0.4 and 0.7% (P = NS) in the PESDA plus RTMCE and control groups, respectively, and in the lungs they were 2.1 and 1.1%, respectively (P = NS). In this canine model, myocardial perfusion imaging obtained with PESDA and RTMCE was safe, with no alteration in cardiac rhythm or left ventricular function. Mild and focal myocardial and pulmonary microhemorrhages were observed in both groups, and may be attributed to surgical tissue manipulation.

Nonsurgical transthoracic epicardial catheter ablation to treat recurrent ventricular tachycardia occurring late after myocardial infarction.

OBJECTIVES: We sought to evaluate feasibility, safety and results of transthoracic epicardial catheter ablation in patients with ventricular tachycardia occurring late after an inferior wall myocardial infarction. BACKGROUND: Transthoracic epicardial catheter ablation effectively controls recurrent ventricular tachycardia (VT) in patients with Chagas' disease in whom epicardial circuits predominate. Epicardial circuits also occur in postinfarction VT. METHODS: Fourteen consecutive patients aged 53.6 +/- 14.5 years with postinfarction VT related to the inferior wall were studied. The VT cycle length was 412 +/- 51 ms. Two patients had previously undergone unsuccessful standard endocardial radiofrequency energy (RF) ablation. The VT was incessant in one patient. Left ventricular angiography showed inferior akinesia in 13 patients and an inferior aneurysm in 1 patient. Ablation was performed with a regular steerable catheter placed into the pericardial sac by pericardial puncture. RESULTS: The pericardial space was reached in all patients. Electrophysiologic evidence of an epicardial circuit was present in 7 of 30 VTs. Due to a high stimulation threshold, empirical thermal mapping was the only criterion used to select the site for ablation. Three VTs were interrupted during the first RF pulse. Two pulses were necessary to render it noninducible in 3 patients (1 VT per patient). In the remaining 4 VTs, 3, 3, 4 and 5 RF pulses, respectively, were used. The overall success was 37.14% (95% confidence interval, 11.83% to 62.45%). Patients are asymptomatic for 14 +/- 2 months. CONCLUSIONS: Postinfarction pericardial adherence does not preclude epicardial mapping and ablation to control VT related to an epicardial circuit in postinferior wall myocardial infarction.

Coronary angioplasty results in leukocyte and platelet activation with adhesion molecule expression. Evidence of inflammatory responses in coronary angioplasty.

OBJECTIVES: This study sought to characterize leukocyte and platelet activation and adhesion molecule expression after coronary angioplasty. BACKGROUND: Coronary angioplasty can be regarded as a clinical model of postischemic inflammation because this intervention leads to the release of inflammatory mediators as a result of plaque rupture and endothelial injury. METHODS: In 13 patients with stable angina (mean [ +/- SEM] age 56.0 +/- 2.4 years, range 44 to 79), blood samples were drawn from the aorta and coronary sinus immediately before and immediately and 15 min after coronary angioplasty. Subsequently, leukocyte and platelet functions were determined. Eleven control patients (57.5 +/- 2.3 years, range 52 to 78) underwent coronary arteriography. RESULTS: Coronary arteriography and angioplasty showed no difference in number of leukocytes between the coronary sinus and the aorta. However, 15 min after coronary angioplasty, there was an increase in neutrophil CD18 and CD11b, monocyte CD14 and platelet glycoprotein IIb/IIIa expression and a decrease in neutrophil L-selectin expression (189 +/- 25%, 163 +/- 27%, 158 +/- 35%, 141 +/- 22% and 31 +/- 10%, respectively, p < 0.01). In the control subjects, no change in adhesion molecule expression occurred. Superoxide production and aggregation in ex vivo-stimulated neutrophils collected from the coronary sinus 15 min after coronary angioplasty was significantly decreased compared with that after coronary arteriography (54 +/- 12% vs. 106 +/- 30% and 58 +/- 11% vs. 102 +/- 29%, respectively, p < 0.01). The reduced responses to phorbol ester stimulation may be explained by previous in vivo activation of neutrophils during coronary angioplasty. CONCLUSIONS: Coronary angioplasty increases neutrophil, monocyte and platelet adhesion molecule expression and induces a significant decrease in ex vivo-stimulated neutrophil superoxide generation and aggregation. These findings suggest that coronary angioplasty triggers cellular activation with an inflammatory response that could contribute to restenosis.

Effect of sexual steroids on the calcium content of aortic atherosclerotic plaque of oophorectomized rabbits.

We determined the effect of conjugated equine estrogen plus medroxyprogesterone acetate on calcium content of aortic atherosclerotic lesions in oophorectomized adult New Zealand rabbits submitted to a cholesterol rich diet. Five groups of 10 animals each were studied: G1 = control, G2 = cholesterol diet only, G3 = diet plus conjugated equine estrogen (0.625 mg/day); G4 and G5 = diet, conjugated equine estrogen (0.625 mg/day) plus medroxyprogesterone acetate (5 and 10 mg/day, respectively). Mean weight varied from 2.7 +/- 0.27 to 3.1 +/- 0.20 kg (P = 0.38) between groups at the beginning and 3.1 +/- 0.27 to 3.5 +/- 0.20 kg (P = 0.35) at the end of the experiment. Cholesterol and triglyceride levels were determined at the time of oophorectomy, 21 days after surgery (time 0), and at the end of follow-up of 90 days. The planimetric method was used to measure plaque and caryometric method for histopathologic examination of the aorta. Calcium content was determined by the method of von Kossa. A similar increase in cholesterol occurred in all treated groups without differences between them at the end of the study. Groups G4 and G5 had smaller areas of atherosclerotic lesions (2.33 +/- 2.8 and 2.45 +/- 2.1 cm(2), respectively) than the groups receiving no progestogens (G2: 5.6 +/- 4 and G3: 4.6 +/- 2.8 cm(2); P = 0.02). The relation between lesion area and total aorta area was smaller in groups treated with combined drugs compared to the groups receiving no progesterone (G4: 14.9 +/- 13 and G5: 14.2 +/- 13.4 vs G2: 35.8 +/- 26 and G3: 25 +/- 8 cm(2), respectively; P = 0.017). Oral conjugated equine estrogen (0.625 mg/day) plus medroxyprogesterone acetate (5 or 10 mg/day) provoked a greater reduction in atherosclerotic plaque area and calcium content in treated groups, suggesting a dose-dependent effect.

Assessment of the cardiovascular effects of electroconvulsive therapy in individuals older than 50 years.

To evaluate the impact of electroconvulsive therapy on arterial blood pressure, heart rate, heart rate variability, and the occurrence of ischemia or arrhythmias, 38 (18 men) depressive patients free from systemic diseases, 50 to 83 years old (mean: 64.7 +/- 8.6) underwent electroconvulsive therapy. All patients were studied with simultaneous 24-h ambulatory blood pressure and Holter monitoring, starting 18 h before and continuing for 3 h after electroconvulsive therapy. Blood pressure, heart rate, heart rate variability, arrhythmias, and ischemic episodes were recorded. Before each session of electroconvulsive therapy, blood pressure and heart rate were in the normal range; supraventricular ectopic beats occurred in all patients and ventricular ectopic beats in 27/38; 2 patients had non-sustained ventricular tachycardia. After shock, systolic, mean and diastolic blood pressure increased 29, 25, and 24% (P < 0.001), respectively, and returned to baseline values within 1 h. Maximum, mean and minimum heart rate increased 56, 52, and 49% (P < 0.001), respectively, followed by a significant decrease within 5 min; heart rate gradually increased again thereafter and remained elevated for 1 h. Analysis of heart rate variability showed increased sympathetic activity during shock with a decrease in both sympathetic and parasympathetic drive afterwards. No serious adverse effects occurred; electroconvulsive therapy did not trigger any malignant arrhythmias or ischemia. In middle-aged and elderly people free from systemic diseases, electroconvulsive therapy caused transitory increases in blood pressure and heart rate and a decrease in heart rate variability but these changes were not associated with serious adverse clinical events.

The effects of gemfibrozil upon the metabolism of chylomicron-like emulsions in patients with endogenous hypertriglyceridemia.

OBJECTIVE: To evaluate the effects of gemfibrozil upon the intravascular metabolism of chylomicron-like emulsions in endogenous hypertriglyceridemia. METHODS: We evaluated the plasma kinetics of a chylomicron-like emulsion in 39 subjects: 27 hypertriglyceridemics, total cholesterol (TC) expressed as median (%25; %75) 7.47 (6.1; 8.19) mmol/l and plasma triglycerides (TG) 4.28 (3.6; 18.5) mmol/l and in 12 normolipidemics, TC 4.7 (3.85; 5.37) mmol/l and TG 0.91 (0.64; 1.75) mmol/l. Hypertriglyceridemics were evaluated at baseline and after a 30-day 1200-mg/day gemfibrozil (n=8) or placebo treatment (n=7). The emulsion labelled with 14C-cholesteryl oleate (14C-CO) and 3H-triolein (3H-TO) was injected intravenously after a 12-h fast. The plasma kinetics of 3H-TO and 14C-CO were determined to assess, respectively, lipolysis and clearance of chylomicron and remnants by compartmental analysis. RESULTS: The residence times (in minutes) of 3H-TO and 14C-CO of hypertriglyceridemics were roughly twice the values of normolipidemics, i.e. 8.0 (5.5; 12.0) versus 15.0 (11.0; 24.0) and 21.5 (14.0; 33.0) versus 44.0 (32.0; 72.0), P=0.001. Gemfibrozil treatment of hypertriglyceridemic patients reduced the residence times of 3H-TO and 14C-CO, respectively, by 46% (P=0.003) and 53% (P=0.008). Effects were noted on the slow phase of emulsion plasma removal, which was reduced in hypertriglyceridemics. After treatment, the emulsion residence times determined in hypertriglyceridemics attained the values of the normolipidemic group. CONCLUSIONS: Gemfibrozil treatment normalised the defects in chylomicron-like emulsion catabolism observed in endogenous hypertriglyceridemia patients.

Effects of etofibrate upon the metabolism of chylomicron-like emulsions in patients with coronary artery disease.

Slow chylomicron intravascular catabolism has been associated with coronary artery disease and screening for drugs that can speed-up this process can be important. In this study, the effects of etofibrate upon chylomicron metabolism was tested by determination of the plasma kinetics of a chylomicron-like emulsion model in 12 patients with coronary artery disease, aged 59+/-11 years, (total cholesterol: 240+/-41 mg/dl; triglycerides: 188+/-42 mg/dl) submitted to a randomized, crossover, double-blind, placebo-controlled study with administration of 1 g per day etofibrate or placebo for 1-month. A 1-month washout period was inserted between the treatment periods. Patients were intravenously injected a chylomicron-like emulsion doubly labeled with 14C-cholesteryl oleate and 3H-triolein at baseline and after treatments. After etofibrate treatment, there was decrease of total cholesterol and triglyceride plasma levels and a trend to increase high-density lipoprotein cholesterol plasma levels. Etofibrate elicited 62% enhancement of post-heparin lipolytic activity and 100% increase of 3H-triglyceride fractional clearance rate compared with placebo treatment. 14C-cholesterol ester fractional clearance rate was 260% greater after etofibrate than after placebo. Therefore, a potent effect of etofibrate on both chylomicron lipolysis and remnant removal was achieved, indicating that this drug can be used to improve this metabolism in future prospective studies.

Effect of simvastatin on monocyte adhesion molecule expression in patients with hypercholesterolemia.

Increased monocyte adherence to the vessel wall is one of the earliest events in atherosclerosis. The mechanism by which hypercholesterolemia causes alterations in endothelial adhesiveness for monocytes is unclear. This study sought to determine if monocyte adhesion molecule expression is affected by low-density lipoprotein (LDL)-cholesterol levels. Patients with hypercholesterolemia and stable coronary artery disease were compared with those without major cardiovascular risk (control). Patients with hypercholesterolemia were treated with simvastatin 20--40 mg/day for 8--10 weeks. Blood samples were examined with flow cytometry assays at baseline and after cholesterol-lowering therapy. Monocyte CD11b and CD14 adhesion molecule expression, measured as fluorescence intensity, were significantly (P<0.0001) higher in hypercholesterolemic patients before the study (176.9+/-9.8 and 138.0+/-4.8, respectively) when compared with that in control subjects (97.2+/-8.1 and 84.0+/-6.4, respectively). Both decreased markedly with treatment: to 118.8+/-6.9 and 103.1+/-3.9, respectively. Monocyte L-selectin expression was significantly lower in patients with hypercholesterolemia before treatment (43.0+/-3.0) when compared with control subjects (79.9+/-2.7), and it increased markedly with treatment (54.2+/-2.5). LDL levels correlated directly with both CD11b and CD14 expression and correlated inversely with L-selectin expression. These data show that hypercholesterolemia affects monocyte adhesion molecule expression which, in turn, decreases with statin-induced plasmatic cholesterol reduction. Such perturbations in monocyte function likely represent a proinflammatory response to hypercholesterolemia and may have a role in the early progression of atherogenesis.

Two- to eight-year survival rates in patients who refused coronary artery bypass grafting.

One hundred and fifty patients with coronary artery disease (CAD) who refused bypass grafting were followed prospectively from 2 to 8 years. Mean age was 57 +/- 8 (standard deviation) years. Ejection fraction averaged 70 +/- 14%. Eight percent of patients had 1-vessel CAD and 92% had multiple-vessel CAD. Medical treatment included propranolol, nifedipine, isosorbide dinitrate, dipyridamole and aspirin. Annual mortality was 0% for 1- and 2-vessel CAD and 1.3% for left main equivalent disease, 3-vessel and left main CAD. Treatment significantly reduced the incidence of stable and unstable angina. Fifty-two patients (34%) had a second hemodynamic study 4.2 +/- 1.3 years after initial evaluation. Stenosis progression or new significant obstructions (greater than or equal to 70%) in previously normal coronary arteries occurred in 61% of 123 arteries studied, whereas new occlusions were observed in 12% of the arteries. Nonfatal acute myocardial infarction incidence was 8%. No significant changes occurred in ejection fraction. In conclusion, proper medical treatment in selected patients with advanced CAD but preserved ventricular function is associated with good long-term survival and remission of symptoms, although progression of coronary atherosclerosis does occur in some patients.

Effect of niacin and etofibrate association on subjects with coronary artery disease and serum high-density lipoprotein cholesterol <35 mg/dl.

Niacin treatment (alone) was compared with etofibrate and niacin combination to treat patients with high-density lipoprotein <35 mg/dl and without hypertriglyceridemia. The niacin and etofibrate combination proved to be safe and increased high-density lipoprotein cholesterol levels to 48%, which was 3 times higher than that obtained with niacin alone.

Additional reduction in blood pressure after cholesterol-lowering treatment by statins (lovastatin or pravastatin) in hypercholesterolemic patients using angiotensin-converting enzyme inhibitors (enalapril or lisinopril).

Blood pressure (BP) reduction was compared between patients receiving angiotensin-converting enzyme inhibitors alone and patients receiving these medications plus statins after 3 months of dietary intervention. Although BP was similarly reduced at week 4, the statin-treated group had a greater reduction in BP and total cholesterol levels at week 16, suggesting a synergistic effect between cholesterol lowering with statins and angiotensin-converting enzyme inhibitor treatment for hypertensive patients.

Effect of pravastatin on plasma removal of a chylomicron-like emulsion in men with coronary artery disease.

The speed of the plasma removal of chylomicrons, the lipoproteins that carry dietary lipids absorbed in the intestine, may influence atherogenesis. Thus, the effects of a 30-day pravastatin or placebo treatment on the plasma kinetics of chylomicron-like emulsions were evaluated in 25 patients with coronary artery disease who were not hypertriglyceridemic in a randomized, single-blinded study. Eleven patients (53 +/- 4 years, 10 men) received pravastatin 40 mg/day and 14 received placebo (52 +/- 3 years, 13 men). Emulsions labeled with triolein ((3)H-TO) and cholesteryl oleate ((14)C-CO) to assess lipolysis and clearance of chylomicron and remnants, respectively, were injected intravenously in a bolus after a 12-hour fast. Blood samples were collected during 60 minutes to determine radio isotope decaying curves and fractional catabolic rates. Subjects were studied at baseline and after the treatment period. Compared with placebo (data expressed as mean +/- SEM), pravastatin treatment increased the (14)C-CO fractional catabolic rates (70 +/- 45% vs 18 +/- 10%, p = 0.01), reduced total cholesterol (-21 +/- 3% vs -3 +/- 2% p = 0.0001), low-density lipoprotein (LDL) cholesterol (-25 +/- 5% vs 4 +/- 6%, p = 0.0001), and apolipoprotein B levels (-22 +/- 3% vs -7 +/- 3% p = 0.01). (3)H-TO fractional catabolic rates, plasma triglycerides, very-low-density lipoprotein (VLDL) cholesterol and high-density lipoprotein (HDL) cholesterol variations did not differ between the groups. The fractional catabolic rate of (14)C-CO was inversely correlated with plasma apolipoprotein B levels (r = -0.7, p = 0.04). This suggests that besides reducing LDL cholesterol, pravastatin also increases chylomicron remnant clearance, with possible antiatherogenic implications.

Hemodynamic effects of intravenous administration of amiodarone in congestive heart failure from chronic Chagas' disease.

Fourteen patients with congestive heart failure due to chronic Chagas' disease had hemodynamic studies before and 20, 40 and 60 minutes and 24 hours after intravenous amiodarone. Amiodarone was given initially as a bolus (5 mg/kg); after 1 hour a continuous infusion was maintained for 24 hours (total dose 900 to 1,050 mg). During the first hour of observation, heart rate and cardiac index decreased and mean right atrial, left ventricular end-diastolic pressures and pulmonary and systemic vascular resistances increased. Except for heart rate and mean right atrial pressure, all hemodynamic variables returned to control values at 24 hours. Thus, myocardial depression occurred with a dose of 5 mg/kg within the first hour of intravenous administration. Amiodarone must be cautiously administered by bolus, especially in patients with cardiac failure.

Cholesterol lowering with statins reduces exercise-induced myocardial ischemia in hypercholesterolemic patients with coronary artery disease.

Coronary flow reserve is mainly influenced by the combination of luminal stenosis and vascular dilation capacity. Thus, after statin treatment, the reduction of ischemic threshold in patients submitted to exercise testing could be intensely influenced by angiographic severity. In this study, we verify the effect of statin treatment on exercise-induced myocardial ischemia in hypercholesterolemic patients with a broad range of coronary angiographic severities. Patients with 2 consecutive positive exercise tests, coronary stenosis > or =70%, total cholesterol > or =300 mg/dl, and triglycerides < or =200 mg/dl were randomly assigned to a 16-week treatment period with either diet alone (n = 39) or diet plus statins (simavastatin, n = 31 and pravastatin, n = 10). Statin-treated patients had a significant variation in total cholesterol (-46% vs -2.7%; p <0.01), low-density lipoprotein cholesterol (-58% vs 0.8%; p <0.01), and high-density cholesterol (+28% vs -6%; p <0.05) in comparison with the diet-only group. After 16 weeks of treatment, 36 patients (92%) in the diet group still had positive exercise tests, whereas only 7 patients (15%) of the statin group had a positive test (p <0.01). The proportion of positive tests was significantly reduced in subgroups of patients with 1-, 2-, or 3-vessel disease. Regarding the severity of coronary stenosis, the proportion of positive tests was significantly reduced in patients with stenosis between 70% and 90% and in patients with stenosis > or =90%. Moreover, the proportion of positive tests tended to decrease to a greater extent in patients with mild coronary disease. In conclusion, cholesterol-lowering treatment with statins reduces exercise-induced myocardial ischemia in hypercholesterolemic patients with mild or severe epicardial coronary stenosis.

Angiotensin-converting enzyme and apolipoprotein B polymorphisms in coronary artery disease.

The association between angiotensin-converting enzyme (ACE) as well as apolipoprotein B polymorphisms and dyslipidemia and coronary artery disease (CAD) is controversial. We assessed the distribution of ACE insertion and/or deletion, apolipoprotein B signal peptide insertion and/or deletion, and apolipoprotein B XbaI restriction fragment length polymorphisms in 388 nondiabetic patients. We studied 112 patients with angiographically defined asymptomatic CAD or with stable functional classes I and II angina and 139 patients with acute myocardial infarction who were age matched to 137 control subjects. Univariate analysis showed higher prevalence of Xba50% reduction of lumen diameter. Overall, multivariable regression disclosed traditional risk factors and elevated levels of apolipoprotein B for men and reduced levels of apolipoprotein AI for women as independent variables for CAD. After adjustment for the most important subset of risk factors (age, hypertension, hypercholesterolemia, and smoking), apolipoprotein B XbaI polymorphism was disclosed as an independent variable for CAD. Apolipoprotein B XbaI was also selected as an independent variable for acute myocardial infarction after adjusting for age, hypertension, hypercholesterolemia, and smoking. Thus, in addition to traditional coronary risk factors, apolipoproteins B and AI, and apolipoprotein B XbaI polymorphism could be considered predictors of CAD.

Effect of spironolactone on ventricular arrhythmias in congestive heart failure secondary to idiopathic dilated or to ischemic cardiomyopathy.

Epidemiologic studies have shown an important increase in the high mortality of patients with congestive heart failure (CHF) despite optimal medical management. Ventricular arrhythmia was recognized as the most common cause of death in this population. Electrolyte imbalance, myocardial fibrosis, left ventricular dysfunction, and inappropriate neurohumoral activation are presumed responsible for sudden cardiac death. In this study, we focused on the deleterious effects of the overproduction of aldosterone that occurs in patients with CHF. Secondary hyperaldersteronism can be part of several factors thought to be responsible for sudden cardiac death. We randomized 35 patients (32 men, aged 48 +/- 9 years) with systolic dysfunction (ejection fraction 33 +/- 5%) and New York Heart Association class III CHF secondary to dilated or ischemic cardiomyopathy into 2 groups. The treatment group received spironolactone, an aldosterone receptor antagonist, along with standard medical management using furosemide, angiotensin-converting enzyme inhibitors, and digoxin. The control group received only the standard medical treatment. Holter monitoring was used to assess the severity of ventricular arrhythmia. After 20 weeks, patients who received spironolactone had a reduced hourly frequency of ventricular premature complexes (VPCs) (65 +/- 18 VPCs/hour at week 0 and 17 +/- 9 VPCs/hour at week 16) and episodes of nonsustained ventricular tachycardia (VT) (3.0 +/- 0.8 episodes of VT/24-hour period at week 0, and 0.6 +/- 0.3 VT/24-hour period at week 16). During monitored treadmill exercise, a significant improvement in ventricular arrhythmia was found in the group receiving spironolactone (39 +/- 10 VPCs at week 0, and 6 +/- 2 VPCs at week 16). These findings suggest that aldosterone may contribute to the incidence of ventricular arrhythmia in patients with CHF, and spironolactone helps reduce this complication.

Clinical predictors of prognosis in severe aortic stenosis in unoperated patients > or = 75 years of age.

In elderly patients with severe aortic stenosis, clinical evaluation can dictate decision making. Asymptomatic patients in normal sinus rhythm, without left atrial enlargement and without bundle branch block, can be safely followed clinically, regardless of echocardiographic findings.

Diltiazem improves left ventricular systolic function following acute myocardial infarction treated with streptokinase. The Calcium Antagonist in Reperfusion Study (CARES) Group.

The role of diltiazem on left ventricular systolic function was analyzed in 101 patients with acute myocardial infarction treated with streptokinase, being obtained, for the total of the population, higher LV global ejection fraction (p = 0.022), LV regional shortening (p = 0.046) and LV global shortening (p = 0.064) for the treated group, relative to the placebo group; the p values were, respectively, 0.005, 0.009, and 0.012, for patients that achieved TIMI-3 antegrade coronary flow. It is concluded that diltiazem is useful as adjuvant to streptokinase, especially when antegrade coronary blood flow TIMI-3 is obtained.