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Objectives: This study was designed to assess the prevalence of major cardiovascular risk factors in familial premature coronary artery disease (P-CAD), affecting two or more siblings within one sibship., Background: Premature CAD has a genetic component. It remains to be established whether familial P-CAD is due to genes acting independently from major cardiovascular risk factors., Methods: We recruited 213 P-CAD survivors from 103 sibships diagnosed before age

Objectives: This study was designed to assess the efficacy and safety of amlodipine, a long-acting calcium channel blocker, in patients with vasospastic angina., Background: Previous studies have established the value of short-acting calcium channel blockers in the treatment of coronary spasm., Methods: Fifty-two patients with well documented vasospastic angina were entered into the present study. After a single-blind placebo run-in period, patients were randomized (in a double-blind protocol) to receive either amlodipine (10 mg) or placebo every morning for 4 weeks. Twenty-four patients received amlodipine and 28 received placebo. All patients were given diaries in which to record both the frequency, severity, duration and circumstances of anginal episodes and their intake of sublingual nitroglycerin tablets., Results: The rate of anginal episodes decreased significantly (p = 0.009) with amlodipine treatment compared with placebo and the intake of nitroglycerin tablets showed a similar trend. Peripheral edema was the only adverse event seen more frequently in amlodipine-treated patients. No patient was withdrawn from the double-blind phase of the study because of an adverse event. Patients who completed the double-blind phase as responders to amlodipine or as nonresponders to placebo were offered the option of receiving amlodipine in a long-term, open label extension phase. During the extension, the daily dose of amlodipine was adjusted to 5 or 15 mg if needed and the rate of both anginal episodes and nitroglycerin tablet consumption showed statistically significant decreases between baseline and final assessment., Conclusion: This study suggests that amlodipine given once daily is efficacious and safe in the treatment of vasospastic angina.

The impact of right bundle branch block on long-term prognosis after anterior wall myocardial infarction is unclear. In 932 patients with Q wave anterior infarction, the short- and long-term prognostic significance of the presence of right bundle branch block was analyzed. Compared with 754 patients without block, 178 patients with right bundle branch block after myocardial infarction showed an increased incidence of left ventricular failure (72% versus 52%, p less than 0.001) and increased in-hospital (32% versus 8%, p less than 0.001) and 1 year after hospital discharge (17% versus 7%, p less than 0.001) cardiac mortality rates. The presence of right bundle branch block was an independent predictor of increased in-hospital and 1-year mortality when entered in a multivariate analysis. However, the absence of left ventricular failure identified a subgroup of patients with right bundle branch block with low in-hospital (4%) and 1 year postdischarge (5%) cardiac mortality rates comparable with those of patients with neither failure nor right bundle branch block (1.7% and 4.8%, respectively). In the presence of left ventricular failure, patients with associated right bundle branch block had higher in-hospital (43% versus 14%, p less than 0.01) and 1 year postdischarge (24% versus 9%, p less than 0.01) cardiac mortality rates than those of patients with failure but no right bundle branch block. Thus, the presence of right bundle branch block after anterior myocardial infarction is an independent marker of poor prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Little is known concerning late outcome and prognostic factors after acute myocardial infarction in the very elderly (greater than 75 years of age). Accordingly, this study compared the clinical course and mortality rate for up to 1 year in a large multicenter data base that included 702 patients greater than 75 years of age (mean +/- SD 81 +/- 4 years), with a less elderly subset of 1,321 patients between 65 and 75 years of age (mean 70 +/- 3 years). The postdischarge 1 year cardiac mortality rate was 17.6% for those greater than 75 years of age compared with 12.0% for patients between 65 and 75 years of age (p less than 0.01). There were differences in the prevalence of several factors, including female gender, history of angina pectoris, history of congestive heart failure, smoking habits and incidence of congestive heart failure during hospitalization. Multivariate analyses of predictors of cardiac death in hospital survivors selected different factors as important in the two age subgroups; age was selected in the 65 to 75 year age group but was not an independent predictor in the very elderly. The survival curves beginning at day 10 for patients 65 to 75 and in those greater than 75 years old were similar for up to 90 days but diverged later. In the very elderly, 63% of late cardiac deaths were sudden or due to new myocardial infarction, similar to the causes of 67% of deaths in the younger age group.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular sensitivity to catecholamines was assessed in 15 patients with hypothyroidism (mean [+/- SEM] thyroxine [T4] index 2.7 +/- 0.5 micrograms/100 ml, thyroid stimulating hormone [TSH] 136.9 +/- 48.3 microU/ml), aged 45 +/- 4 years and in 8 healthy control subjects. The study was repeated in 10 patients with hypothyroidism 4.0 +/- 0.5 months after thyroid replacement therapy (T4 index 9.9 +/- 2.1 micrograms/100 ml, TSH 3.5 +/- 1.3 microU/ml). In addition, basal, average and maximal heart rates were measured using 24 h ambulatory electrocardiographic (ECG) monitoring, and plasma levels of epinephrine and norepinephrine were determined before and after thyroid replacement. Heart rate increased less after bolus injection of 0.8, 1.6 and 3.2 micrograms of isoproterenol in the hypothyroid (10 +/- 2, 15 +/- 2 and 21 +/- 4 beats/min, respectively) than in the euthyroid (16 +/- 3, 22 +/- 3 and 30 +/- 4 beats/min, respectively) state (p less than 0.05). Control subjects reacted similarly to patients receiving thyroid replacement. Basal heart rate (64 +/- 3 versus 68 +/- 3 beats/min, p less than 0.05) and maximal heart rate (116 +/- 5 versus 133 +/- 5 beats/min, p less than 0.05) were lower on 24 h ambulatory ECG monitoring in the hypothyroid than euthyroid state despite higher basal plasma norepinephrine levels (394 +/- 45 versus 315 +/- 45 pg/ml, p less than 0.05). Thus, patients with hypothyroidism display a decreased cardiac chronotropic response to beta-adrenergic stimulation. This may contribute in part to the decreased basal and maximal daily heart rates seen in patients with hypothyroidism, which occurs despite elevated plasma norepinephrine levels.

The use of planar radionuclide ventriculography to evaluate global and segmental ventricular function is limited by the superimposition of structures in some projections and the gross segmental resolution of the planar technique. Preliminary reports have suggested the feasibility of tomographic gated radionuclide ventriculography with rotating detector systems. This study tested the hypotheses that 1) tomographic radionuclide ventriculography detects segmental dysfunction at rest not identified with multiview planar studies and single plane contrast ventriculography, and 2) ventricular volumes and ejection fraction calculated from these studies provide data similar to those obtained with angiography and planar radionuclide ventriculography. Gated blood pool tomograms were acquired over 180 degrees at 15 frames per cardiac cycle during the initial 90% of the cardiac cycle. Compared with the multiview planar technique tomographic ventriculography showed an increased sensitivity for detecting left ventricular segments with significant coronary artery stenosis (97 versus 74%, p less than 0.025) without any loss in specificity. Compared with both planar radionuclide and contrast ventriculography, tomographic radionuclide ventriculography also detected more noninfarcted left ventricular segments supplied by stenosed coronary arteries (81 versus 39 and 32%, respectively, p less than 0.01). Tomographic radionuclide ventriculographic measurements of left ventricular volumes and ejection fraction showed close correlations with angiographic and planar radionuclide determinations. Gated blood pool tomography is a sensitive method for the evaluation of segmental wall motion and an accurate method for the measurement of global left ventricular volumes and ejection fraction.

Whether ventricular fibrillation occurring within 48 h after acute myocardial infarction is associated with particular clinical features and poor prognosis, especially in patients with anterior myocardial infarction, is still debated. Therefore, clinical variables and in-hospital and 1 year mortality rates were analyzed in 2,088 patients, aged 18 to 95 years (mean +/- SD 64 +/- 12), admitted to the hospital with acute myocardial infarction between 1979 and mid 1984. One hundred forty-seven patients (7%) had at least one episode of ventricular fibrillation occurring within 48 h of hospital admission. Of these, 25% died during their initial hospitalization compared with 13% of patients without early ventricular fibrillation (p less than 0.001). In greater than 50% of patients with early ventricular fibrillation, the immediate cause of death was left ventricular failure or cardiogenic shock. In contrast, the 1 year mortality rate after hospital discharge was not significantly greater in patients with than in those without early ventricular fibrillation (15 versus 11%, respectively), particularly in the subgroup of patients with anterior myocardial infarction in which the mortality rate tended to be lower in patients with early ventricular fibrillation (8 versus 14%, respectively). Similar mortality results were found when only primary (not associated with left ventricular failure) ventricular fibrillation was analyzed. The left ventricular ejection fraction and the incidence of complex ventricular arrhythmias from 24 h ambulatory electrocardiographic monitoring obtained at hospital discharge were not different in survivors with or without early ventricular fibrillation (0.45 +/- 0.13 versus 0.49 +/- 0.14 and 41 versus 41%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

A family is described in which nine members over two generations had an aortic dissecting aneurysm or aortic or arterial dilation at a young age. The family has been followed up since 1977 after the death of a second teenager from a kindred of 11. None of the patients had the Marfan syndrome or a history of systemic hypertension. Three members died of ruptured aortic dissecting aneurysm and acute hemopericardium at 14, 18 and 24 years of age, respectively; a fourth member died suddenly at age 48 years, a few years after aortic repair for aneurysmal dilation. One member underwent surgical repair of an ascending aortic dissecting aneurysm at age 18 years and is still alive. Four members are currently under close medical observation for aortic or arterial dilation. Histologic examination of the aortic wall at autopsy or surgery in three patients revealed a loss of elastic fibers, deposition of mucopolysaccharide-like material in the media and cystic medial changes. Types I and III collagen from cultured fibroblasts appeared normal on gel electrophoresis. Results of indirect immunofluorescent studies of the elastin-associated microfibrillar fiber array in skin and fibroblast culture from multiple family members were also normal. This dramatic familial cluster of aortic dissecting aneurysm and aortic or arterial dilation suggests a genetically determined disease of autosomal dominant inheritance although the basic defect remains unknown.

Previous studies suggested that cigarette smoking 1) inhibits an increase in coronary blood flow that should occur with increased myocardial oxygen demands, and 2) alters thromboxane and prostacyclin production, causing vasoconstriction and platelet aggregation. In 38 smokers (26 men and 12 women, aged 50 +/- 8 years [mean +/- standard deviation] ) with coronary artery disease, systemic and coronary hemodynamic and serologic variables were measured before and after smoking two cigarettes (in 8 to 10 minutes) (21 patients) or 8 to 10 minutes without smoking (17 patients; control group). No variable changed in the control group. Smoking increased (p less than 0.05) heart rate-systolic pressure product, cardiac output and maximal first derivative of left ventricular pressure (dP/dt) without significantly changing the coronary sinus concentrations of thromboxane B2 or 6-keto-prostaglandin F1 alpha (the stable metabolites of thromboxane A2 and prostacyclin, respectively). Smoking did not increase coronary flow in 6 of 11 patients with greater than 70% stenosis of the proximal left anterior descending or circumflex coronary artery, or both, whereas it caused an increase in coronary flow in all 10 patients without proximal stenoses (p = 0.006). To determine if smoking altered the response of coronary flow to increased myocardial oxygen demands, 10 smokers (5 men and 5 women, aged 48 +/- 9 years) underwent atrial pacing for 5 minutes followed 15 minutes later by atrial pacing for 5 minutes during smoking. In the five patients without proximal left coronary artery stenoses, coronary flow increased 26 +/- 29 ml/min with pacing and 45 +/- 21 ml/min with pacing/smoking (p = 0.018).(ABSTRACT TRUNCATED AT 250 WORDS)

Whether thyroid replacement therapy can trigger cardiac arrhythmias in patients with hypothyroidism is not known. In this prospective study, 24 h ambulatory electrocardiographic (ECG) monitoring was used to assess the frequency of atrial and ventricular premature beats in 25 patients with hypothyroidism (5 men and 20 women, aged 56 +/- 3 years) before and 3.5 +/- 0.5 months (mean +/- SEM) after thyroid replacement therapy. Plasma thyroid-stimulating hormone was 73.6 +/- 12.3 and 3.1 +/- 0.6 microU/ml and free thyroxine index was 2.4 +/- 0.4 and 9.8 +/- 0.9 micrograms/100 ml at baseline and after thyroid replacement therapy, respectively. The frequency of ventricular premature beats was not affected by thyroid replacement therapy (from 273 +/- 221 at baseline to 352 +/- 235 beats/24 h after therapy), even in patients with frequent baseline arrhythmias. In contrast, the frequency of atrial premature beats was slightly increased after thyroid replacement therapy (from 47 +/- 17 to 279 +/- 197 beats/24 h), largely as a result of changes seen in three patients. No patient developed new onset of sustained ventricular or supraventricular arrhythmias. Average, basal and maximal heart rates during ECG monitoring increased significantly after thyroid replacement therapy (average 72 +/- 2 to 80 +/- 2; basal 64 +/- 2 to 70 +/- 2; maximal 114 +/- 3 to 130 +/- 3 beats/min, respectively, p less than 0.001). In conclusion, thyroid replacement therapy is safe in patients with common benign cardiac arrhythmias, and does not trigger an increase in arrhythmia frequency except in rare patients with baseline atrial premature beats. It is, however, associated with an increase in basal, average and maximal heart rates.

Some studies have reported increased short-term mortality and higher incidence of multivessel coronary artery disease in patients with inferior myocardial infarction and complete heart block, but information is lacking on clinical outcome after hospital discharge. Therefore, data were obtained and analyzed in 749 patients who were admitted with inferior myocardial infarction to four different centers and followed up for 1 year. Six hundred fifty-four patients (Group 1) did not have complete heart block and 95 (Group 2) had complete heart block during their hospital stay (incidence rate 12.8%). Compared with Group 1, Group 2 patients were older (66 versus 61 years, p less than 0.01), more often had signs of left ventricular failure (p less than 0.001) and had higher peak creatine kinase values (1,840 versus 1,322 IU/liter, p less than 0.001). The in-hospital mortality rate was higher in Group 2 than in Group 1 (24.2 versus 6.3%, p less than 0.001). However, at discharge there was no difference between Group 1 and Group 2 in clinical characteristics, left ventricular ejection fraction (0.52 +/- 0.12 versus 0.52 +/- 0.11) or incidence of complex ventricular arrhythmias on ambulatory electrocardiographic monitoring. Furthermore, during the year after hospital discharge, patients in Groups 1 and 2 did not have significantly different mortality rates (6.4 versus 10.1%, p = NS). The incidence rate of reinfarction (4%) was the same in Groups 1 and 2. The incidence of coronary artery bypass surgery was slightly but not significantly higher in Group 1 compared with Group 2 (11 versus 4%).(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the changes in right heart hemodynamics and geometry early after surgery for chronic pulmonary hypertension due to large vessel thromboembolic occlusion, 30 patients were evaluated 8 +/- 8 days (mean +/- SD) before and 6 +/- 4 days after pulmonary thromboendarterectomy by two-dimensional echocardiography and right heart catheterization. Surgery resulted in an early significant improvement in hemodynamic variables including mean pulmonary artery pressure (48 +/- 12 to 28 +/- 8 mm Hg, p less than 0.001), right ventricular systolic pressure (76 +/- 20 to 47 +/- 15 mm Hg, p less than 0.001), pulmonary vascular resistance (935 +/- 620 to 278 +/- 252 dynes.s.cm-5, p less than 0.001) and cardiac index (2.0 +/- 0.5 to 2.9 +/- 0.6 liters/min per m2, p less than 0.001). Similarly, echocardiographic variables of right heart structures, which were well outside the normal range preoperatively, improved significantly early after thromboendarterectomy. These included diameters of the pulmonary artery (2.8 +/- 0.3 to 2.4 +/- 0.4 cm, p less than 0.001), inferior vena cava (2.9 +/- 0.6 to 2.2 +/- 0.4 cm, p less than 0.001) and right atrium (6.8 +/- 1.5 to 5.9 +/- 1.5 cm, p less than 0.001) as well as right ventricular short axis (4.5 +/- 0.8 to 3.7 +/- 0.8 cm, p less than 0.001) and long axis (8.7 +/- 0.9 to 8.1 +/- 0.9 cm, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Densitometric regional ejection fraction obtained by computer analysis of digital subtraction ventriculography was evaluated as a new, quantitative, three-dimensional index of regional left ventricular performance. Eighteen patients with coronary artery disease and seven control subjects had right anterior oblique ventriculography at rest and immediately after rapid atrial pacing using central venous injection of contrast material. Regional left ventricular ejection fraction was determined by densitometry in six segments drawn around the end-diastolic center of gravity, and compared with two conventional indexes of segmental wall motion: area and radial regional ejection fraction. Densitometric, area or radial regional ejection fraction was classified as abnormal if it fell at least 2 standard deviations below the corresponding mean value in the normal group. The densitometric method did not require outlining of the end-systolic left ventricular silhouette and was the easiest and fastest to perform of all three techniques. In addition, intra- and interobserver reproducibilities were higher with the densitometric method (r = 0.97 and 0.95) than with either the area (r = 0.84 and 0.82) or the radial method (r = 0.82 and 0.76). Regional left ventricular dysfunction as assessed by the densitometric, area and radial techniques allowed the detection of coronary artery disease in 50, 50 and 44% of the patients at rest and in 83, 67 and 61% of the patients in the post-pacing period, respectively. Post-pacing regional left ventricular dysfunction accurately predicted the presence or absence of greater than 70% diameter stenosis in the supplying coronary artery in 75, 67 and 56% of the cases, respectively. Thus, densitometric analysis of digital subtraction ventriculography allows a fast and reproducible three-dimensional determination of regional left ventricular ejection fraction. Using this technique, pacing-induced regional dysfunction can be detected in most patients with coronary artery disease and corresponds well with the location of significant coronary artery lesions.