Showing papers in "American Journal of Cardiology in 1994"
TL;DR: It is suggested from data that waist circumference values above approximately 100 cm, or abdominal sagittal diameter values > 25 cm are most likely to be associated with potentially "atherogenic" metabolic disturbances.
Abstract: The amount of abdominal visceral adipose tissue measured by computed tomography is a critical correlate of the potentially "atherogenic" metabolic disturbances associated with abdominal obesity. In this study conducted in samples of 81 men and 70 women, data are presented on the anthropometric correlates of abdominal visceral adipose tissue accumulation and related cardiovascular disease risk factors (triglyceride and high-density lipoprotein cholesterol levels, fasting and postglucose insulin and glucose levels). Results indicate that the waist circumference and the abdominal sagittal diameter are better correlates of abdominal visceral adipose tissue accumulation than the commonly used waist-to-hip ratio (WHR). In women, the waist circumference and the abdominal sagittal diameter also appeared more closely related to the metabolic variables than the WHR. When the samples were divided into quintiles of waist circumference, WHR or abdominal sagittal diameter, it was noted that increasing values of waist circumference and abdominal sagittal diameter were more consistently associated with increases in fasting and postglucose insulin levels than increasing values of WHR, especially in women. These findings suggest that the waist circumference or the abdominal sagittal diameter, rather than the WHR, should be used as indexes of abdominal visceral adipose tissue deposition and in the assessment of cardiovascular risk. It is suggested from these data that waist circumference values above approximately 100 cm, or abdominal sagittal diameter values > 25 cm are most likely to be associated with potentially "atherogenic" metabolic disturbances.
2,094 citations
TL;DR: The low prevalence of AF in the absence of clinical and subclinical cardiovascular disease calls into question the existence and clinical usefulness of the concept of so-called "lone atrial fibrillation" in the elderly.
Abstract: Atrial fibrillation (AF) is a common arrhythmia in elderly persons and a common cause of embolic stroke. Most studies of the prevalence and correlates of AF have used selected, hospital-based populations. The Cardiovascular Health Study is a population-based, longitudinal study of risk factors for coronary artery disease and stroke in 5,201 men and women aged > or = 65 years. AF was diagnosed in 4.8% of women and in 6.2% of men at the baseline examination, and prevalence was strongly associated with advanced age in women. Prevalence of AF was 9.1% in men and women with clinical cardiovascular disease, 4.6% in patients with evidence of subclinical but no clinical cardiovascular disease, and only 1.6% in subjects with neither clinical nor subclinical cardiovascular disease. A history of congestive heart failure, valvular heart disease and stroke, echocardiographic evidence of enlarged left atrial dimension, abnormal mitral or aortic valve function, treated systemic hypertension, and advanced age were independently associated with the prevalence of AF. The low prevalence of AF in the absence of clinical and subclinical cardiovascular disease calls into question the existence and clinical usefulness of the concept of so-called "lone atrial fibrillation" in the elderly.
1,104 citations
TL;DR: The results suggest that the presence of mismatch in patients with CAD and severe LV dysfunction is associated with poor annual survival with medical therapy, and Revascularization in Patients with PET mismatch appears to be associated with improved survival and heart failure symptoms.
Abstract: Patients with coronary artery disease (CAD) and severe left ventricular (LV) dysfunction have a high but variable annual mortality and some may benefit from myocardial revascularization. This study aimed to evaluate the prognostic value of positron emission tomography (PET), and its interrelation with the choice of medical therapy or revascularization for predicting survival and improvement in symptoms of heart failure in patients with CAD and LV dysfunction. Ninety-three consecutive patients with angiographic CAD and a mean LV ejection fraction of 0.25 who underwent cardiac PET studies for assessment of hypoperfused yet viable myocardium (“mismatch pattern”) using N-13 ammonia and 18-F deoxyglucose were followed up for an average of 13.6 months. Fifty patients underwent medical treatment and 43 underwent revascularization. The Cox model analysis showed that the extent of mismatch had a negative effect (p = 0.02), whereas revascularization had a positive effect on survival (p = 0.04). The annual survival probability of patients with mismatch receiving medical therapy was lower than of those without mismatch (50 vs 92%, p = 0.007). Patients with mismatch who underwent revascularization had a higher survival rate than those treated medically (88 vs 50%, p = 0.03). The presence of mismatch also predicted improvement in heart failure symptoms after revascularization (p
500 citations
TL;DR: The responsiveness to clinical change of the Seattle Angina Questionnaire (SAQ), a disease-specific measure for CAD, was compared with that of the Short Form-36, a generic measure of health status.
Abstract: Monitoring the outcomes of treatment and quantifying patients' functional status have assumed a prominent role in both clinical trials and quality assurance programs. Because patients with coronary artery disease (CAD) may have comorbid illnesses, and because generic health status questionnaires may not focus on symptoms and impairments unique to coronary disease, a generic measure of health status may not be sufficient to detect important changes in patients' CAD. The responsiveness to clinical change of the Seattle Angina Questionnaire (SAQ), a disease-specific measure for CAD, was compared with that of the Short Form-36, a generic measure of health status. Both questionnaires were serially administered, 3 months apart, to 45 patients undergoing coronary angioplasty and to 130 patients with stable CAD. Most scales of both questionnaires improved significantly after coronary angioplasty. The responsiveness statistics of the SAQ exceeded those of the Short Form-36. Among 130 patients with initially stable angina, 33 deteriorated, 79 remained stable, and 18 improved over 3 months of observation. Mean SAQ scores changed significantly and appropriately in each of these groups. In contrast, none of the Short Form-36 scales detected these more subtle changes. Although useful in assessing overall function, a generic health status measure, such as the Short Form-36, may not be responsive enough to detect important clinical changes in patients' CAD. A disease-specific instrument, such as the SAQ, can be an important and relevant outcome measure in clinical trials or quality assurance programs.
420 citations
TL;DR: Analysis of gender-related differences in cardiac dimensions showed that female athletes had smaller LV diastolic cavity dimension and smaller wall thickness than males of the same age and body size who were training in the same sport.
Abstract: In the present study, we used echocardiography to investigate the morphologic adaptations of the heart to athletic training in 947 elite athletes representing 27 sports who achieved national or international levels of competition. Cardiac morphology was compared for these sports, using multivariate statistical models. Left ventricular (LV) diastolic cavity dimension above normal (> 54 mm, ranging up to 66 mm) was identified in 362 (38%) of the 947 athletes. LV wall thickness above normal (> 12 mm, ranging up to 16 mm) was identified in only 16 (1.7%) of the athletes. Athletes training in the sports examined showed considerable differences with regard to cardiac dimensions. Endurance cyclists, rowers, and swimmers had the largest LV diastolic cavity dimensions and wall thickness. Athletes training in sports such as track sprinting, field weight events, and diving were at the lower end of the spectrum of cardiac adaptations to athletic training. Athletes training in sports associated with larger LV diastolic cavity dimensions also had higher values for wall thickness. Athletes training in isometric sports, such as weightlifting and wrestling, had high values for wall thickness relative to cavity dimension, but their absolute wall thickness remained within normal limits. Analysis of gender-related differences in cardiac dimensions showed that female athletes had smaller LV diastolic cavity dimension (average 2 mm) and smaller wall thickness (average 0.9 mm) than males of the same age and body size who were training in the same sport.(ABSTRACT TRUNCATED AT 250 WORDS)
399 citations
TL;DR: Prolonged QRS duration and increased dispersion of repolarization make independent contributions to the risk of arrhythmic cardiac death in patients with coronary artery disease.
Abstract: In a recent prospective study of myocardial ischemia, arrhythmic cardiac death occurred in 17 of 936 patients (2%) during a 2-year follow-up after acute myocardial infarction or unstable angina. Dispersion of ventricular repolarization was evaluated on the 12-lead electrocardiogram at enrollment in 17 patients who subsequently died of cardiac arrhythmia and in 51 matched survivors. The aim of this study was to evaluate the relation between various measurements of dispersion of repolarization and subsequent arrhythmic cardiac death, and to determine if dispersion of repolarization makes an independent contribution to the risk of arrhythmic cardiac death. Ventricular depolarization quantitated in terms of mean QRS (QRS-m) duration, and ventricular repolarization quantitated in terms of mean (m), maximal-minimal dispersion (d), standard deviation (s), and coefficient of variation (cv) of QT and JT intervals, were determined. Univariate analyses revealed that 2 standard electrocardiographic parameters, QRS-m and QT-m, and 3 dispersion variables, JT-d, JT-s, and JTc-d, were associated with arrhythmic cardiac death (p < 0.01). Multivariate analyses revealed that the combination of the dispersion parameter (JT-d, JT-s, or JTc-d) and QRS-m made an independent contribution to the risk of arrhythmic cardiac death. The findings highlight the importance of both delayed depolarization and heterogenous repolarization as risk factors for arrhythmic cardiac death. Thus, increased dispersion of repolarization is associated with an elevated likelihood of arrhythmic cardiac death. Prolonged QRS duration and increased dispersion of repolarization make independent contributions to the risk of arrhythmic cardiac death in patients with coronary artery disease.
342 citations
TL;DR: The data showed that CAD, PAD, and ABI were more prevalent in men than in women aged ≥62 years, and that CAD was also present in 53% and PAD in 33% of the population.
Abstract: Our data showed that CAD, PAD, and ABI were more prevalent in men than in women aged ≥62 years. Of our 1,886 patients, only 705 (37%) had no CAD, PAD, or ABI. CAD was present in 43%, PAD in 25%, and ABI in 26% of our population. If ABI was present, CAD was also present in 53% and PAD in 33% of our population. If PAD was present, CAD was also present in 58% and ABI in 34% of our population. If CAD was present, ABI was also present in 32% and PAD in 33% of our population.
317 citations
TL;DR: The analysis of standard 12-lead surface electrocardiographic tracings obtained in 127 persons including 50 subjects without structural heart disease and 77 patients presenting with acute myocardial infarction found that QT dispersion in persons without heart disease averaged 30 +/- 10 ms compared with 56 +/- 24 ms in patients with acuteMyocardial Infarction.
Abstract: QT dispersion (defined as maximal QT interval minus minimal QT interval) as assessed on the surface electrocardiogram has been demonstrated to reflect regional inhomogeneity of ventricular repolarization. However, the variability of repeated QT dispersion measurements has not been validated in a prospective study. Thus, the present study is based on the analysis of standard 12-lead surface electrocardiographic (ECG) tracings obtained in 127 persons including 50 subjects without structural heart disease and 77 patients presenting with acute myocardial infarction. RR and QT intervals were measured by means of a digitizer tablet and QT/QTc dispersion was subsequently calculated automatically by PC-based analysis software. Measurements were obtained on 2 separate occasions by the same observer to assess the intraobserver variability. In addition, all tracings were evaluated by a second investigator to determine the interobserver variability. QT dispersion in persons without heart disease averaged 30 +/- 10 ms compared with 56 +/- 24 ms in patients with acute myocardial infarction (p < 0.0001). Patients with infarction who developed ventricular fibrillation within the first 24 hours after admission (11 of 77) had an even larger QT dispersion of 88 +/- 30 ms (p < 0.0001). Repeated measurements of QT dispersion in all 127 subjects revealed a correlation coefficient of 0.91 for both intra- and interobserver variability. Similar results were obtained for repeated determination of QTc dispersion (r = 0.93 and r = 0.90, respectively). When only patients with infarction were considered, correlation coefficients between 0.84 and 0.88 were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)
262 citations
TL;DR: Assessment of the immediate and short-term results of anterograde transcatheter closure of the patent ductus arteriosus using single or multiple Gianturco coils for ducts < 3.3 mm in diameter and of angiographic type B found immediate complete closure in 33 patients.
Abstract: Retrograde coil embolization of the patent ductus arteriosus (PDA) has been reported for ducts
237 citations
TL;DR: Sensitivity of electrocardiography progressively increased from the first to the fourth quartile of left ventricular mass in subjects with echocardiographic LVH, and its performance was superior to that of Sokolow-Lyon voltage in a receivers' characteristic curve analysis.
Abstract: This study was aimed at improving the performance of standard electrocardiographic criteria of left ventricular hypertrophy (LVH) in essential hypertension using echocardiographic left ventricular mass as reference. In 923 white, untreated hypertensive subjects (mean age 51, prevalence of echocardiographic LVH 34%), sensitivity of electrocardiographic criteria of LVH varied between 9% and 33% and specificity was generally > or = 90%. The sum of Sv3 + RaVL (Cornell voltage) showed the closest association with echocardiographic left ventricular mass (r = 0.48, p 2.4 mV in men and > 2.0 mV in women), that yielded a good combination between sensitivity (26% in men and 19% in women, overall 22%) and specificity (96% in men and 95% in women, overall 95%). When LVH at electrocardiography was defined as the positivity of at least 1 of the following 3 criteria--Sv3 + RaVL > 2.4 mV in men or > 2.0 mV in women, a typical strain pattern, or a Romhilt-Estes point score > or = 5--sensitivity increased to 39% in men and 29% in women (overall 34%) and specificity decreased to 94% in men and 93% in women (overall 93%). Sensitivity of electrocardiography progressively increased from the first to the fourth quartile of left ventricular mass in subjects with echocardiographic LVH.(ABSTRACT TRUNCATED AT 250 WORDS)
235 citations
TL;DR: The Probucol Quantitative Regression Swedish Trial tested whether treatment of hypercholesterolemic persons with probucol for 3 years affected femoral atherosclerosis and found no difference between the treatment groups with regard to change in arterial edge roughness or amount of aorto-femoral Atherosclerosis.
Abstract: The Probucol Quantitative Regression Swedish Trial tested whether treatment of hypercholesterolemic persons with probucol for 3 years affected femoral atherosclerosis. The primary end point was the change in atheroma volume estimated as change in lumen volume of the femoral artery assessed by quantitative arteriography. Three hundred three patients with visible atherosclerosis were randomized to probucol 0.5 g, twice daily, or to placebo. All patients were given diet and cholestyramine, 8 to 16 g/day. Twenty-nine patients were excluded because of inadequate primary end point measurements. The mean age of the remaining 274 subjects (158 were men) was 55 years. Seventeen percent had intermittent claudication and 24% had angina pectoris. After 3 years, the probucol-treated patients had 17% lower serum cholesterol, 12% lower low-density lipoprotein cholesterol, 24% lower total high-density lipoprotein cholesterol, and 34% lower high-density lipoprotein2 cholesterol levels than control subjects. All lipoprotein differences between the treatment groups remained highly significant during the trial. There was no statistically significant change in lumen volume between the probucol and the control group. Furthermore, there was no difference between the treatment groups with regard to change in arterial edge roughness or amount of aorto-femoral atherosclerosis; neither were there any differences between the treatment groups with regard to change in ST-segment depressions on exercise tests or ankle/arm blood pressure (secondary end points). In the control group, lumen volume increased (p < 0.001) and roughness of the femoral artery decreased (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: TCD reliably detects paradoxical cerebral embolism through a patent foramen ovale, and provides important additional information for evaluating its clinical relevance by semi-quantification of embolic contrast material.
Abstract: The prevalence of a patent foramen ovale was assessed by simultaneously performing transesophageal contrast echocardiography and transcranial contrast Doppler sonography (TCD) in 137 subjects (mean age 36 years) with stroke of unclarified etiology (n = 41), clarified etiology (n = 33), and in normal subjects (n = 63; mean age 32 years). Patent foramen ovale was found significantly more often in patients with unclarified than clarified strokes or in normal subjects (66% vs 33%, or 43%). Massive paradoxical embolism through a patent foramen ovale, identified by TCD, occurred significantly (p < 0.01) more often in patients with unclarified (64%) than clarified (27%) strokes or in normal subjects (3%). However, minimal shunts were typical in normal subjects (79%). Patent foramen ovale was detected indirectly by TCD when calculated on the basis of transesophageal contrast echocardiographic findings (sensitivity 89%, specificity 92%). Thus, TCD reliably detects paradoxical cerebral embolism through a patent foramen ovale, and provides important additional information for evaluating its clinical relevance by semiquantification of embolic contrast material.
TL;DR: Controversy persists regarding whether oxygen radicals contribute to extending cell death following reperfusion and whether reperFusion itself causes cell death, and the resolution of this controversy nor the availability of clinical therapies to reduce reperfusions-induced cell death is likely in the near future.
Abstract: Experimental studies have demonstrated that reperfusion is associated with a host of distinctive pathophysiologic derangements, the most important of which are reperfusion arrhythmias, transient mechanical dysfunction or "myocardial stunning," and cell death. Reperfusion arrhythmias and myocardial stunning occur in experimental animals after transient ischemia followed by reperfusion, and there is considerable evidence that these derangements also develop in humans, although the existence of malignant reperfusion arrhythmias in humans remains uncertain. Reperfusion arrhythmias and myocardial stunning can be considered manifestations of sublethal, reversible cellular injury. The pathogenesis of reperfusion arrhythmias and stunning has not been conclusively established; however, there is considerable evidence that generation of oxygen radicals and perturbations of calcium homeostasis play an important role. Antioxidants and calcium antagonists have been shown to mitigate these manifestations of reperfusion injury. In contrast, the likelihood of lethal reperfusion-induced injury remains highly controversial. Although many studies have reported reduction of infarct size with antioxidants, numerous others have failed to reproduce these results. Consequently, intense controversy persists regarding whether oxygen radicals contribute to extending cell death following reperfusion and whether reperfusion itself causes cell death. Neither the resolution of this controversy nor the availability of clinical therapies to reduce reperfusion-induced cell death is likely in the near future.
TL;DR: Coronary calcium determined by electron beam computed tomography has the potential to predict segmental histopathologic coronary disease.
Abstract: Coronary calcium determined by electron beam computed tomography (CT) has not been systematically evaluated regarding prediction of histopathologic atherosclerotic disease. Furthermore, gender specificity has not been examined. The 3 major epicardial arteries were dissected from 13 consecutive hearts (5 women and 8 men) after autopsy. Each artery was straightened and scanned using CT in contiguous 3 mm thick cross sections. After imaging, histologic sections were prepared at corresponding intervals and luminal area obstruction determined by planimetry. Electron beam CT scans were analyzed to determine coronary calcium area (i.e., tomographic area with CT density > 130 Hounsfield units). A total of 522 histologic specimens were examined and paired with corresponding CT scans (182 in women, 340 in men). Receiver-operating characteristic (ROC) analysis was used to define site specificity of calcium area for luminal area narrowing by atherosclerosis. ROC curve areas for segmental CT calcium and prediction of atherosclerosis representing mild, moderate, or severe disease were, respectively, 0.712, 0.843, and 0.857 for women and 0.732, 0.793, and 0.841 for men. Curves relating false-positive rate (1-specificity) to predefined degrees of atherosclerotic narrowing versus calcium area were curvilinear. In both women and men, calcium areas on the order of 1 mm2/coronary segment were necessary to predict at least mild atherosclerosis with a false-positive rate of 0% (i.e., 100% specificity), whereas a calcium area > 3 mm2 was necessary to predict the same result for severe disease. In conclusion, coronary artery calcium area as determined by electron beam CT has the potential to predict segmental histopathologic coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: Results indicate that beta-blocker administration has important effects on RR interval variability and on its spectral components, and the observed reduction in signs of sympathetic activation and the increase in vagal tone after beta blockade help to explain the beneficial effects of these drugs after myocardial infarction.
Abstract: This study analyzed, with spectral techniques, the effects of atenolol or metoprolol on RR interval variability in 20 patients 4 weeks after the first uncomplicated myocardial infarction. Beta blocker-induced bradycardia was associated with a significant increase in the average 24-hour values of RR variance (from 13,886 +/- 1,479 to 16,728 +/- 1,891 ms2) and of the normalized power of the high-frequency component (from 22 +/- 1 to 28 +/- 2 normalized units), whereas the low-frequency component was greatly reduced (from 60 +/- 3 to 50 +/- 3 normalized units). When considering day and nighttime separately, the effects of both drugs were more pronounced in the daytime. In addition, a marked attenuation was observed in the circadian variation of the low-frequency component after beta blockade. As a result, the early morning increase of the spectral index of sympathetic modulation was no longer detectable. These results indicate that beta-blocker administration has important effects on RR interval variability and on its spectral components. The observed reduction in signs of sympathetic activation and the increase in vagal tone after beta blockade help to explain the beneficial effects of these drugs after myocardial infarction. However, the potential clinical relevance of the increase in RR variance remains to be established.
TL;DR: Four inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase have been approved for treatment of hypercholesterolemia, three of which are fungal metabolites or derivatives thereof: lovastatin, simvastsatin, and pravastatin.
Abstract: Four inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase have been approved for treatment of hypercholesterolemia. Three of these are fungal metabolites or derivatives thereof: lovastatin, simvastatin, and pravastatin. The fourth, fluvastatin, is totally synthetic. Its structure, containing a fluorophenyl-substituted indole ring, is distinct from that of the fungal metabolites. Lovastatin and simvastatin are administered as prodrugs, which undergo in vivo transformation to active inhibitory forms; fluvastatin and pravastatin are administered as active agents. The HMG-CoA reductase inhibitors are all effective in reducing plasma concentrations of low density lipoprotein. They have differing pharmacokinetic properties, which may be of importance in some patients. All of these drugs are very well tolerated, and there do not appear to be major differences in toxicity or adverse effects. When LDL reductions > 30% are needed, simvastatin is the most cost-effective HMG-CoA reductase inhibitor. However, these drugs are most commonly used in dosages that reduce LDL-C by 20-30%. For this degree of LDL reduction, fluvastatin is the most cost-effective HMG-CoA reductase inhibitor.
TL;DR: Investigation of gender-related differences in LV and myocardial function in 65 patients with aortic stenosis who underwent cardiac catheterization and echocardiography found significant differences between men and women with regard to LV geometry and function.
Abstract: In aortic stenosis, gender and other differences in the adaptive remodeling of the left ventricle have been described, but the influence of left ventricular (LV) geometry on systolic function is not widely appreciated. This study tested the hypothesis that the increased ejection fraction seen in some elderly women with aortic stenosis is due to changes in LV geometry, not increased myocardial mass or enhanced myocardial function. We therefore investigated gender-related differences in LV and myocardial function by analysis of end-systolic circumferential stress versus shortening relations in 65 patients (29 men and 36 women) with aortic stenosis who underwent cardiac catheterization and echocardiography. Despite similar degrees of aortic stenosis, there were significant differences between men and women with regard to LV geometry and function. When compared with men, women had higher peak LV pressures (205 +/- 27 vs 188 +/- 27 mm Hg, p < 0.01), higher ejection fractions (66 +/- 14% vs 57 +/- 18%, p < 0.05), smaller LV end-diastolic dimensions (43 +/- 8 vs 51 +/- 6 mm, p < 0.01) and higher relative wall thickness (0.66 +/- 0.27 vs 0.50 +/- 0.10, p < 0.01). LV mass was similar in the 2 groups. Mean values for stress were lower in women and there was a predominance of women at extremely low levels of stress; this subgroup had very high values for relative wall thickness and endocardial shortening, but overall stress-shortening relations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The absence of pulmonary edema in these patients in the nitroprusside study reinforces the importance of selective nitric oxide effects in pulmonary circulation.
Abstract: The mechanism of increased pulmonary wedge pressure and cardiac output after nitric oxide inhalation is not clear. Nitric oxide is rapidly inactivated by hemoglobin before it can produce systemic effects. 3 Thus, selective nitric oxide pulmonary vasodilator effects led to these preliminary results. The hypothesis is that acute reduction in right ventricular afterload caused an acute increment of right ventricular cardiac output. The acute increment of blood return to the impaired left ventricle not associated with reduction in afterload caused the increase in wedge pressure and consequently pulmonary edema. In addition, acute reduction in right ventricular afterload could lead to redistribution of blood volume to pulmonary circulation. The absence of pulmonary edema in these patients in the nitroprusside study reinforces the importance of selective nitric oxide effects in pulmonary circulation.
TL;DR: The accuracy of a simple physical activity questionnaire and readily available clinical data in predicting subsequent treadmill performance was examined and a nomogram was developed, which yields a reasonably accurate estimate of a patient's exercise capacity.
Abstract: Recent investigations suggested that clinical exercise testing can be optimized by individualizing the protocol, depending on the purpose of the test and the subject tested This requires some knowledge of a patient's exercise capacity before beginning the test The accuracy of a simple physical activity questionnaire and readily available clinical data in predicting subsequent treadmill performance was examined A brief, self-administered questionnaire (VSAQ) was developed for veterans who were referred to exercise testing for clinical reasons The VSAQ was designed to determine which specific daily activities were associated with symptoms of cardiovascular disease (fatigue, chest pain and shortness of breath) Two hundred twelve consecutive patients (mean age 62 +/- 8 years) referred for maximal exercise testing were studied Clinical and demographic variables were added to VSAQ responses in a stepwise regression model to determine their ability to predict treadmill performance Only metabolic equivalents by VSAQ, and age were significant predictors of treadmill performance; these 2 variables yielded R = 082 (SEE 143; p < 0001), and explained 67% of the variance in exercise capacity The regression equation reflecting the relation between age, VSAQ and exercise capacity was: achieved metabolic equivalents = 47 + 097 (VSAQ) - 006 (age) Using this equation, a nomogram was developed Incorporating the VSAQ with the nomogram requires only a few minutes, and yields a reasonably accurate estimate of a patient's exercise capacity Although the present equation is population-specific, a similar approach in different populations may be useful for individualizing protocols for clinical exercise testing
TL;DR: The purpose of this study was to evaluate the effects of atrioventricular junction radiofrequency ablation on the quality of life, exercise performance, and echocardiographic parameters in 23 patients with chronic, severely symptomatic, drug-refractory atrial fibrillation or flutter.
Abstract: The purpose of this study was to evaluate the effects of atrioventricular junction radiofrequency ablation on the quality of life, exercise performance, and echocardiographic parameters in 23 patients with chronic, severely symptomatic, drug-refractory atrial fibrillation or flutter. Initially, patients were randomized to receive ablation plus pacemaker therapy (n = 12) or pacemaker therapy alone (n = 11). After 15 days, palpitations decreased by 92% and 37% (p = 0.004), rest dyspnea by 79% and 40% (p = NS), effort dyspnea by 65% and 30% (p = 0.03), exercise intolerance by 54% and 17% (p = 0.005), and asthenia by 67% and 31% (p = 0.02) in the 2 groups, respectively. At the end of this short-term study, control patients also underwent ablation therapy, and a 3-month intrapatient followup study was performed in 22 patients. New York Heart Association functional class ≥3 was present in 14 patients (64%) before, but in only 3 patients (14%) after ablation therapy (p = 0.002); specific activity scale functional class ≥3 was present in 9 patients (41%) before, but in only 5 (23%) after ablation therapy (p = NS). Exercise duration during standardized stress testing increased by a mean of 63 ± 93 seconds (15% increase) (p = 0.001). In the 9 patients with depressed left ventricular systolic function, echocardiographic fractional shortening increased by 34% (from 23 ± 5% to 31 ± 9%) (p = 0.003). In the remaining 13 patients with normal systolic function, fractional shortening decreased by 10% (from 40 ± 5% to 36 ± 6%) (p = 0.05). In conclusion, radiofrequency ablation of the atrioventricular junction ameliorates quality of life and physical performance; left ventricular systolic function improves in patients with depressed cardiac performance at initial evaluation.
TL;DR: Patients with unstable angina and no critical coronary obstruction had an excellent short-term prognosis and nearly one third of the patients without critical coronary stenosis had impaired angiographic filling, suggesting a possible pathophysiologic role for coronary microvascular dysfunction.
Abstract: Previous studies have reported that some patients presenting with unstable angina are found at coronary angiography to have no critical coronary stenosis. This study evaluated the clinical presentation and arteriographic findings in patients enrolled in the Thrombolysis in Myocardial Ischemia (TIMI-IIIA) trial, which assessed the effect of tissue-type plasminogen activator added to conventional therapy on the coronary arteriographic findings in patients presenting with ischemic pain at rest. Three hundred ninety-one patients were enrolled in the TIMI-IIIA trial and underwent coronary arteriography within 12 hours of enrollment. Fifty-three patients (14%) had no luminal diameter stenosis of a major coronary artery of > or = 60% on the baseline arteriogram. Compared with patients with unstable angina with an identifiable culprit lesion, patients without critical coronary obstruction were more likely to be women and non-white and less likely to have ST-segment deviation on the presenting electrocardiogram. Arteriography in such patients revealed no visually detectable coronary stenosis in half of the group; the remaining patients had noncritical coronary narrowing (i.e., < 60% luminal diameter stenosis) without morphologic features (ulceration or thrombus) suggestive of unstable or active coronary plaque. Nearly one third of the patients without critical coronary stenosis had impaired angiographic filling, suggesting a possible pathophysiologic role for coronary microvascular dysfunction. These patients with unstable angina and no critical coronary obstruction had an excellent short-term prognosis; 2% died or had myocardial infarction compared with 18% of patients with critical obstruction.
TL;DR: The stressfulness of the transactions that persons high in hostility have with their interpersonal environments suggests an inverse relation between hostility and HF power, which in turn may increase risk of coronary artery disease.
Abstract: Disordered autonomic regulation of the cardiovascular system has been implicated in sudden cardiac death and coronary artery disease in numerous studies. Bigger et al 1 showed that survival after myocardial infarction was predicted by high-frequency (HF) power of the heart period power spectrum, a measure of vagal modulation of RR intervals, 2 by power in other frequency bands, and by the low-frequency (LF) to HF power ratio, a measure that has been used to estimate sympathovagal balance. Increased heart rate, reflecting global cardiac autonomic control, is associated with development of atherosclerosis in animal models 3 and age-adjusted levels of atherogenic lipoproteins in humans. 4 Heart rate-lowering interventions such as surgical ablation of the sinoatrial node and β-adrenergic antagonists have antiatherogenic effects. 3 Cardiovascular regulation by the autonomic nervous system may link negative personality characteristics, e.g., hostility, with increased risk of coronary artery disease, an association generally supported by available data. 5,6 Two views about the nature of the link, the constitutional and the transactional theories, specify different mechanisms. The constitutional theory holds that the autonomie activity associated with risk of coronary artery disease is caused by a constitutional characteristic which also accounts for hostility. 5 In this view, hostility is a marker of factors that influence brainstem cardioregulatory centers. The transactional theory holds that hostile persons interact with their environment in a way that creates interpersonal conflict and reduces social support. 5 Since in laboratory experiments, psychological Stressors decrease HF power in the heart period power spectrum, 7 the stressfulness of the transactions that persons high in hostility have with their interpersonal environments suggests an inverse relation between hostility and HF power, which in turn may increase risk of coronary artery disease.
TL;DR: The influence of current estrogen replacement therapy in postmenopausal women on endothelial-dependent and independent vasomotor responsiveness to acetylcholine is examined to suggest that estrogen plays a fundamentally important role in the relationship between coronary vascular endothelium and vascular smooth muscle.
Abstract: Recently, Williams et al’ reported that acute administration of estrogen attenuates the coronary vasoconstrictor response to acetylcholine in atherosclerotic cynomolgus monkeys. These observations suggest that estrogen plays a fundamentally important role in the relationship between coronary vascular endothelium and vascular smooth muscle. This study examines the influence of current estrogen replacement therapy in postmenopausal women on endothelial-dependent and independent vasomotor responsiveness to acetylcholine. Ten postmenopausal women with exertional angina undergoing routine diagnostic coronary angiography or percutaneous transluminal coronary angioplasty were studied. The protocol was approved by the Clinical Research Practices Committee and each subject gave informed consent before the study, Four women were taking estrogen replacement therapy (PremarinB 0.625 to 1.25 mglday or topical estradiol 0.1 mg). None of the women were taking progesterone. All of the women had minimal coronary artery narrowings in the proximal portion of the left anterior descending or a nondominant circumflex coronary artery. Vasoactive medications were withheld for 12-24 hours before the procedure. A 3Fr infusion catheter was positioned in the proximal left anterior descending or proximal circumflex artery through the guiding catheter. After the baseline angiogram was recorded, 3 consecutive 2-minute infusions of acetylcholine were administered into the proximal coronary artery. The$ow rate (0.8 mllmin) was calculated to deliver a final estimated blood concentration of 10s, 10m7 and 10m6 M. After each acetylcholine infusion, repeat angiography was performed in an identical fashion to baseline. After the third acetylcholine in& sion and angiogram, a 50 pg bolus of nitroglycerin was administered and a final coronary angiogram was recorded. Heart rate, blood pressure and appropriate electrocardiographic leads were monitored during the infusions to verify the absence of any changes in hemodynamic status or evidence of &hernia. Proximal and midvessel segments of the coronary artery distal to the tip of the infusion catheter were analyzed without knowledge of the estrogen status using a quantitative coronary angiography method (Gammasonits, Chicago, Illinois). When possible, coronary segments from the noninfused half of the left coronary distribution
TL;DR: The data confirm the association between low RR variability and mortality after acute myocardial infarction, and suggest that the increased risk of early mortality associated with reduced RR variability reflects an imbalance in sympathovagal function that is unrelated to left ventricular function.
Abstract: The relation between both time and frequency domain analyses of RR variability and mortality was examined in a series of 226 consecutive patients with acute myocardial infarction admitted to 3 district hospitals in London. All patients underwent 24-hour Holter monitoring early after infarction (mean 83 hours, range 48 to 180), and time and frequency domain analyses of RR variability were performed using commercially available software. During an 8-month follow-up period (range 3 to 12 months), there were 19 cardiac deaths (8.4%). Time domain analysis confirmed reduced RR variability (SDRR, SDANN, SD) among nonsurvivors compared with survivors. However, there was no difference between the groups when the percentage of absolute differences between successive RR intervals >50 ms (pNN50) and the root-mean-square of successive differences (RMSSD)—vagal measures of RR variability—were analyzed. Frequency domain analysis demonstrated a significant difference between those who died and the survivors when the low-frequency component—modulated by both vagal and sympathetic mechanisms—was analyzed; however, this was less marked when the high-frequency component—modulated by vagal activity—was analyzed. None of these measures of RR variability was related to infarct site or left ventricular ejection fraction. In conclusion, the data confirm the association between low RR variability and mortality after acute myocardial infarction. However, the mechanism does not appear to relate exclusively to decreased parasympathetic tone. The data suggest that the increased risk of early mortality associated with reduced RR variability reflects an imbalance in sympathovagal function that is unrelated to left ventricular function.
TL;DR: The origins and development of electrocardiography are summarized and its role in defining cardiology as a specialty is addressed and it is addressed how this information helps physicians diagnose various forms of heart disease.
Abstract: The invention of the electrocardiograph by Dutch physiologist Willem Einthoven in 1902 gave physicians a powerful tool to help them diagnose various forms of heart disease, especially arrhythmias and acute myocardial infarction. The discovery of x-rays in 1895 and the invention of the electrocardiograph 7 years later inaugurated a new era in which various machines and technical procedures gradually replaced the physician's unaided senses and the stethoscope as the primary tools of cardiac diagnosis. These sophisticated new approaches provided objective information about the structure and function of the heart in health and disease. This review summarizes the origins and development of electrocardiography and addresses its role in defining cardiology as a specialty.
TL;DR: Serial electrocardiograms revealed diagnostic features of embolism in an additional 3 patients and two-dimensional Doppler echocardiography at admission revealed tricuspid valve regurgitation and an increased right ventricular end-diastolic diameter in all cases.
Abstract: In 49 consecutive patients (27 men and 22 women, age range 44 to 86 years) presenting with acute symptoms and with subsequently proven pulmonary embolism, and without previous lung disease, the 12-lead electrocardiograms obtained at hospital admission were reviewed in a blinded fashion to identify electrocardiographic features suggestive of right ventricular overload. Pulmonary embolism was considered probable in 37 patients (76%), from the presence of > or = 3 of the following abnormalities: (1) incomplete or complete right bundle branch block (n = 33); which was associated with ST-segment elevation (n = 17) and positive T wave (n = 3) in lead V1; (2) S waves in leads I and aVL of > 1.5 mm (n = 36); (3) a shift in the transition zone in the precordial leads to V5 (n = 25); (4) Q waves in leads III and aVF, but not in lead II (n = 24); (5) right-axis deviation, with a frontal QRS axis of > 90 degrees (n = 16), or an indeterminate axis (n = 15); (6) a low-voltage QRS complex of 7 days. In the 12 patients with normal electrocardiograms at admission, serial electrocardiograms revealed diagnostic features of embolism in an additional 3 patients. Two-dimensional Doppler echocardiography at admission revealed tricuspid valve regurgitation and an increased right ventricular end-diastolic diameter in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: Pulmonary hypertension is not uncommon in the echocardiograms of patients with sickle cell disease, but although a substantial number of these patients may not have symptoms of cardiac dysfunction, mortality is significantly increased compared with patients without pulmonary hypertension.
Abstract: Pulmonary hypertension is not uncommon in the echocardiograms of patients with sickle cell disease. Although a substantial number of these patients may not have symptoms of cardiac dysfunction, mortality is significantly increased compared with patients with sickle cell disease hut without pulmonary hypertension.
TL;DR: Patients with severe MR due to mitral valve prolapse, who are asymptomatic or minimally symptomatic with normal ventricular performance, can be expected to progress to surgical indications at an annual rate of 10.3%.
Abstract: The natural history of patients with severe nonischemic mitral regurgitation (MR) from mitral valve prolapse, who are asymptomatic or minimally symptomatic and have normal right ventricular (RV) and left ventricular (LV) performance, has not been evaluated previously. To define natural history in this population and to determine if any objective variables could predict disease progression, 31 patients were followed annually with severe MR due to prolapse, who at entry were asymptomatic or minimally symptomatic and had normal RV and LV performance at rest by radionuclide cineangiography. Average follow-up in patients not reaching surgical end point was 4.7 years. The Kaplan-Meier product limit estimates were used to determine the rate of progression to either “operable” symptoms or to previously defined “high risk” ventricular performance descriptors, if the latter occurred first. Univariate comparisons of Kaplan-Meier curves and multivariate Cox proportional hazards analyses were used to define prognostically important variables measured at entry. Fourteen patients developed symptoms warranting referral for operation; none developed high-risk ventricular performance descriptors. The annual end point risk was 10.3%. Of all covariates, only change in RV ejection fraction from rest to exercise was significantly associated with disease progression. Annual risk of progression to surgical end point was 4.9% in the subgroup in which this parameter increased with exercise and 14.7% in the subgroup without an increase (p = 0.04). Patients with severe MR due to mitral valve prolapse, who are asymptomatic or minimally symptomatic with normal ventricular performance, can be expected to progress to surgical indications at an annual rate of 10.3%. The change in RV ejection fraction during exercise is useful in predicting the likelihood of such progression.
TL;DR: Aortic wall stiffness increased with age and aortic diameter, but at all ages the Marfan group exhibited a stiffer aorta for a given diameter than did the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Abstract: This study examined the relations between age, arterial distensibility, and systemic hemodynamics in patients with the Marfan syndrome. The study group included 170 patients referred to a specialist clinic, of whom 55 (age 26 +/- 12 years) were diagnosed as having Marfan syndrome. The remaining 115 patients (age 25 +/- 14 years) formed a control group. Each patient underwent echocardiographic examination, with measurement of ascending aorta diameter at end-diastole and end-systole, and aortic flow velocities. The elastic properties of the aorta were indexed by calculation of aortic distensibility, wall stiffness, and systemic pulse wave velocity. Mean end-diastolic aortic diameter in the Marfan group (38 +/- 9 mm) was greater than that in the controls (26 +/- 4 mm, p < 0.01). Resting heart rate and aortic flow velocities were similar in the 2 groups, but systemic arterial pulse pressure was greater in the Marfan group (50 +/- 12 mm Hg) than in the controls (41 +/- 8 mm Hg, p < 0.01). Aortic diameter increased with age in both groups, but at all ages the Marfan group exhibited greater aortic diameters (p < 0.05). Aortic distensibility was less in the Marfan group (2.6 +/- 1.3 cm2.dynes-1 x10(-6)) than in the controls (6.2 +/- 2.1 cm2.dynes-1 x 10(-6), p < 0.01), and the aortic wall stiffness index was greater in the Marfan group (7.9 +/- 3.4) than in the controls (2.8 +/- 0.6, p < 0.01). Aortic wall stiffness increased with age and aortic diameter, but at all ages the Marfan group exhibited a stiffer aorta for a given diameter than did the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The CAST results support the secondary preventive benefit of β-blocker therapy in high-risk post-myocardial infarction patients, and calls attention to the possible preventive benefit against proarrhythmic events experienced in the CAST.
Abstract: The Cardiac Arrhythmia Suppression Trial (CAST) showed antiarrhythmic drug suppression of asymptomatic or mildly symptomatic ventricular arrhythmias in survivors of myocardial infarction to be harmful. This study retrospectively searched the CAST results for evidence of mortality and morbidity reduction in patients receiving optional β-blocker therapy. All enrolled (n = 2,611) and suppressed main study (n = 1,735) CAST patients with an ejection fraction of ≤40% were examined using univariate analysis, Kaplan-Meier curves, and a Cox proportional-hazards multivariate analysis with respect to optional β-blocker therapy prescribed at baseline. CAST patients receiving β-blocker therapy had significantly enhanced survival at 30 days, and at 1 and 2 years of follow-up against all-cause and arrhythmic death or nonfatal cardiac arrest. Multivariate analysis showed β-blocker therapy to be independently associated with a one-third reduction in arrhythmic death or cardiac arrest (p = 0.036). In CAST patients with a history of congestive heart failure, β-blocker therapy was independently associated with longer time to occurrence of new or worsened congestive heart failure (p = 0.015). This study supports the secondary preventive benefit of β-blocker therapy in high-risk post-myocardial infarction patients, and calls attention to the possible preventive benefit of β-blocker therapy against proarrhythmic events experienced in the CAST.