Diagnostic accuracy of exercise thallium-201 scintigraphy in men with asymptomatic essential hypertension.

Coronary artery disease is responsible for much of the morbidity and mortality in patients with essential hypertension, and these complications have proven to be relatively resistant to antihypertensive therapy. However, the diagnosis of coronary disease in the hypertensive population has been considered problematic. In the present study, 30 asymptomatic patients with mild to moderate hypertension with positive exercise electrocardiograms (ECG) or stress thallium-201 scintigrams underwent coronary angiography to determine the accuracy of these tests for coronary artery disease. The exercise ECG was positive in 25 subjects, of whom 15 had significant coronary lesions and 10 did not. Thallium-201 scintigraphy proved more accurate: 17 of 18 patients with reversible abnormalities had significant obstructive coronary disease anatomically corresponding to the defect, one patient with a fixed defect had normal coronary arteries and was found to have an idiopathic cardiomyopathy, and 9 of 11 without defects had no significant lesions. The results were similar in populations with and without echocardiographic criteria for left ventricular hypertrophy. These findings indicate that despite previous suggestions to the contrary, thallium-201 scintigraphy can accurately diagnose coronary artery disease in most patients with asymptomatic essential hypertension, and that most asymptomatic hypertensive patients with physiologic evidence of myocardial ischemia have associated coronary artery disease.

What is the role of silent coronary artery disease and left ventricular hypertrophy in the genesis of ventricular arrhythmias in men with essential hypertension?

Ventricular arrhythmias are not uncommon in patients with hypertension, are often attributed to left ventricular hypertrophy and are thought to be associated with an increased risk of sudden death. However, underlying silent coronary artery disease, another potential cause of ventricular arrhythmias, is often present in the same patient group. Therefore, the prevalence of ventricular arrhythmias was prospectively examined in 183 consecutive asymptomatic men with hypertension with neither clinical nor electrocardiographic (ECG) evidence of coronary artery disease in whom technically adequate echocardiograms could be obtained. After previous therapy had been withdrawn for greater than or equal to 4 days, each patient underwent exercise or dipyridamole thallium-201 scintigraphy, 48-h Holter ambulatory ECG monitoring and echocardiography for measurement of the left ventricular mass index. Forty patients (22%) had frequent ventricular ectopic activity, defined on the basis of greater than 10 premature ventricular complexes/h (38 patients) or ventricular tachycardia (11 patients), or both. A higher proportion of patients with than without a reversible thallium-201 defect had frequent premature ventricular complexes (33% vs. 18%, p less than 0.02) or ventricular tachycardia (14% vs. 4%, p less than 0.02). Similarly, more patients with than without left ventricular hypertrophy (defined as left ventricular mass index greater than or equal to 134 g/m2) had frequent premature ventricular complexes (29% vs. 15%, p less than 0.05) and ventricular tachycardia (12% vs. 2%, p less than 0.01). By stepwise logistic regression analysis, both findings were independent predictors of ventricular arrhythmia, which was present in 53% of patients with both abnormalities, but in only 12% of those with neither abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of long-term vasodilator therapy on electrocardiographic abnormalities in chronic aortic regurgitation.

Electrocardiographic abnormalities develop in patients with chronic aortic regurgitation (AR). Although vasodilator drugs may reduce left ventricular (LV) volume overload, the effects of such therapy on electrocardiographic abnormalities have not been previously evaluated. Accordingly, electrocardiograms were analyzed before and after double-blind, randomized administration of either hydralazine or placebo in 54 patients with chronic AR. These patients were without limiting symptoms and had preserved ejection fraction on entry in the study. The magnitude of ST-segment depression and Romhilt-Estes point score for LV hypertrophy were assessed. Baseline ST depression and LV hypertrophy scores in the placebo and hydralazine groups were not significantly different. At follow-up, after a mean of 19 +/- 6 months, there was a significant reduction in ST depression in patients taking hydralazine (n = 28) compared with patients given placebo (n = 26): -0.023 +/- 0.044 vs 0.029 +/- 0.055 mV, respectively (p = 0.0001); and in the LV hypertrophy score (-1.1 +/- 2.2 vs 0.9 +/- 2.3 points, respectively; p = 0.002). Hydralazine-treated patients also had significant decreases in LV end-diastolic and end-systolic volume indexes, and a significant increase in ejection fraction. These results suggest that such vasodilator therapy may be beneficial in patients with chronic AR.

Influence of therapy on silent ischemia and ventricular arrhythmias in hypertensive patients.

To assess whether therapy with hydrochlorothiazide (HCTZ) or the calcium antagonist nitrendipine influences silent ischemia or arrhythmias, we studied 10 asymptomatic hypertensive male patients with positive Tl-201 scintigraphy in a double-blind, crossover protocol. Blood pressure (BP) and 48-h Holter monitoring were obtained after 2 weeks of placebo and 8 weeks each of HCTZ and nitrendipine therapy. Ischemia was defined as greater than 1 mm ST-segment depression lasting greater than 1 min and was quantified by the number of episodes, duration, and area under the curve (AUC). The mean number of PVCs per hour and the number of episodes of ventricular tachycardia (greater than 3 beats) were also assessed. Diastolic BP was significantly reduced by both HCTZ and nitrendipine (98 +/- 6 vs. 90 +/- 6 vs. 88 +/- 7 mm Hg, respectively, p less than 0.05), but systolic BP was unchanged for either drug. The number of ischemic episodes was reduced by nitrendipine, from 2.4 +/- 3 to 0.8 +/- 2, (p less than 0.05) but not by HCTZ (2.4 +/- 3 to 1.5 +/- 3, p = NS). The duration of ischemia (37 +/- 43 vs. 5 +/- 9 min, p less than 0.05) as well as the AUC (41 +/- 45 vs. 7 +/- 14 mm/min, p less than 0.05) were reduced only by nitrendipine. The number of PVCs rose with HCTZ therapy, from 19 +/- 34 to 69 +/- 88 (p less than 0.05) and was unchanged by nitrendipine (19 +/- 34 vs. 19 +/- 40, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Correlates of diastolic filling abnormalities in hypertension: a Doppler echocardiographic study.

Hypertension and aging are both associated with changes of left ventricular (LV) diastolic filling and increased LV mass. To determine whether diastolic filling abnormalities are present in hypertension independent of aging and significant hypertrophy, we studied 19 hypertensive patients following a period of 4 weeks when they were not receiving therapy and 18 normotensive subjects matched for sex, age, and LV mass. All subjects had normal systolic function and ejection fraction as assessed by radionuclide angiography. We measured peak velocity of early filling (E), late filling (A), and their ratio (E/A) by Doppler echocardiography. Filling indices were abnormal in hypertensive patients, but none of the filling indices were significantly correlated with LV mass. E was inversely related to age (r = -0.62; p less than 0.01) and diastolic blood pressure (r = 0.45; p less than 0.05) in normotensive individuals, but these correlations were not significant in hypertensive patients. E was not significantly correlated to LV mass or wall thickness. In contrast, A was influenced by septal wall thickness and blood pressure in both groups. E/A correlated inversely with age in both normal individuals (r = -0.74) and hypertensive patients (r = -0.51). These findings indicate that diastolic filling abnormalities in hypertension are not solely caused by either LV hypertrophy or by aging and therefore must be in part related to the hemodynamic load or altered myocardial or chamber properties.

Left ventricular hypertrophy reversal with labetalol and propranolol: a prospective randomized, double-blind study.

Hypertensive patients with left ventricular hypertrophy (LVH) have increased cardiovascular morbidity and mortality. Experimental studies indicate the importance of both the alpha and beta components of the adrenergic nervous system in the development and reversal of LVH. Therefore labetalol (L), a combined alpha and beta blocker, and propranolol (P), a nonselective beta blocker, were evaluated in a randomized, double-blind study of 35 hypertensive patients with echocardiographic evidence of LVH. Following 2 weeks of placebo, L or P was titrated as needed and tolerated to maximum total daily doses of 1600 mg and 640 mg, respectively. A thiazide diuretic was added if necessary for blood pressure control. M-mode echocardiograms were performed at baseline and after 1, 3, 6, and 12 months of blood pressure control. The echocardiograms were read independently by two blinded observers for end-diastolic dimension and wall thicknesses, and left ventricular mass. Fractional shortening, cardiac output, and peripheral vascular resistance were derived using standard formulas. Both drugs reduced blood pressure significantly and comparably. Significant changes in the echocardiographic measurements were observed as early as 1 month and usually persisted throughout the study. Both drugs decreased posterior wall thickness; however, only the decrease in propranolol group achieved statistical significance. Septal wall thickness was reduced by L at 3 and 12 months. End-diastolic dimension increased significantly in the L-treated group at 3, 6, and 12 months of therapy, whereas P had no effect on this measurement.(ABSTRACT TRUNCATED AT 250 WORDS)

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy.

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.

Usefulness of thallium-201 scintigraphy in predicting the development of angina pectoris in hypertensive patients with left ventricular hypertrophy.

Hypertension and left ventricular (LV) hypertrophy are independent risk factors for the development of coronary artery disease. To determine whether patients at higher risk for coronary artery disease can be identified, 40 asymptomatic hypertensive men with LV hypertrophy were prospectively studied using exercise thallium-201 scintigraphy and exercise radionuclide angiography. Endpoints indicative of coronary artery disease were defined as the subsequent development of typical angina pectoris, which occurred in 8 patients during a median follow-up of 38 months, or myocardial infarction, which did not occur. The exercise electrocardiogram was interpreted by standard ST-segment criteria and by a computerized treadmill exercise score. Abnormal ST-segment responses were present in 16 of the 40 hypertensives (40%), whereas the treadmill score was positive in 8 of those same 40 patients (20%). Scintigraphic perfusion defects assessed both visually and semiquantitatively were observed in 8 of 40 (20%) patients. An abnormal ejection fraction response to exercise was present in 40% (16 of 40) of patients, and 3 of 40 (7.5%) developed new wall motion abnormalities during exercise. Six of 8 patients with either perfusion defects or abnormal treadmill score developed typical angina during follow-up. All 5 patients with concordant positive exercise scintigrams and treadmill score developed chest pain during follow-up and had coronary artery disease confirmed by coronary angiography. However, only 7 of 16 (44%) patients with positive ST changes or abnormal ejection fraction responses during exercise developed chest pain during follow-up. In contrast, of 32 patients with negative scintigrams only 2 developed atypical chest pain syndromes, and significant coronary artery disease was excluded by angiography in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary morbidity and mortality, pre-existing silent coronary artery disease, and mild hypertension.

Experimental findings in animals and epidemiologic studies in humans provide strong evidence that hypertension promotes the onset and progression of atherosclerosis. However, effective antihypertensive therapy has not consistently reduced the incidence of cardiac events in the major trials of treatment for mild hypertension. In reviewing these trials and the recent data on the pathophysiologic interrelationships among hypertension, atherosclerosis, and myocardial ischemia, two factors stand out: First, the power of these trials to produce a positive result was limited because of their size, entry criteria, duration, and other considerations; second, autopsy and epidemiologic data suggest that some patients in these trials probably had advanced coronary artery disease at the time of entry. Because these patients probably developed symptomatic coronary artery disease by virtue of this pre-existing disease, the failure of antihypertensive therapy alone to prevent cardiac events in trials of relatively short duration should not be construed as evidence against its value as a long-term therapy.

Hypertensive heart disease: the critical role of left ventricular hypertrophy.

The presence of left ventricular hypertrophy in hypertensive patients has been linked with increased likelihood for developing congestive heart failure, the potential for myocardial ischemia and the inherent risk for sudden death. In this paper we review current knowledge regarding the role of left ventricular hypertrophy in cardiac morbidity and mortality and emphasize the need for further study to explore the efficacy of pharmaceutical agents in reducing cardiac complications of hypertension in high-risk patients.

Effect of diltiazem on left ventricular mass and diastolic filling in mild to moderate hypertension.

It is still uncertain whether antihypertensive therapy with calcium antagonists in general, and diltiazem in particular, can reduce left ventricular (LV) mass index and improve LV diastolic filling in hypertension. Therefore, 24 patients with mild to moderate hypertension (diastolic blood pressure 95 to 114 mm Hg before therapy) were randomly assigned to receive either a sustained-release preparation of diltiazem (n = 13) or placebo (n = 11) for 16 weeks in a double-blind, parallel-group protocol. M-mode and pulsed Doppler echocardiograms were performed at baseline and at the end of monotherapy. Echocardiograms were read blindly by 2 independent observers. The patients who received placebo exhibited no change in blood pressure, cardiac dimensions or LV function. Diltiazem significantly reduced both systolic pressure (151 +/- 14 to 139 +/- 12 mm Hg) and diastolic pressure (101 +/- 4 to 90 +/- 7 mm Hg, both p less than 0.05). Posterior wall and septal wall thicknesses decreased, but the changes were not statistically significant. End-diastolic dimension was reduced by diltiazem from 53 +/- 5 to 51 +/- 5 mm (p less than 0.05). LV mass index decreased significantly with diltiazem by 10%, from 125 +/- 21 to 113 +/- 23 g/m2 (p less than 0.05). The LV wall thickness to radius ratio remained unchanged during both diltiazem and placebo treatments. Changes in LV mass index and blood pressure did not correlate, suggesting that this response is influenced by factors other than pressure reduction alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term vasodilator therapy of chronic aortic insufficiency. A randomized double-blinded, placebo-controlled clinical trial.

Although vasodilator drugs acutely reduce regurgitation and improve cardiac performance in aortic insufficiency, their long-term effects on left ventricular size and function are uncertain. Consequently, we performed a double-blinded, placebo-controlled trial using hydralazine in 80 minimally symptomatic patients who had clinically stable, moderate-to-severe aortic insufficiency. Patients randomized to hydralazine displayed a progressive reduction in left ventricular end-diastolic volume index (LVEDVI) measured by radionuclide angiography, the predetermined end point of the study. At 24 months, mean LVEDVI had been reduced by 30 +/- 38 ml/m2, an 18% reduction from baseline. In contrast, LVEDVI changed minimally in patients randomized to placebo, and the intergroup differences over time were statistically significant (p less than 0.03). The hydralazine group also experienced reductions in left ventricular end-systolic volume index and increases in ejection fraction that were significantly different (both p less than 0.01) from changes in placebo-treated patients. These findings show that long-term treatment with hydralazine reduces the volume overload in aortic insufficiency and suggest that such therapy may have a beneficial effect on the natural history of the disease.

Systemic hypertension, left ventricular hypertrophy and coronary artery disease.

The potential mechanisms for the development of myocardial ischemia in hypertensive left ventricular (LV) hypertrophy involve changes in the coronary circulation characterized by a reduction of coronary vascular reserve and an acceleration of the atherosclerotic process. This combination of factors is probably reflected in the epidemiologic findings of increased coronary morbidity and mortality in hypertension, particularly when it is associated with LV hypertrophy. The failure of several antihypertensive trials to reduce coronary morbidity and mortality emphasizes the importance of early detection of significant coronary artery disease (CAD) among hypertensive patients with LV hypertrophy. A strategy to detect asymptomatic CAD based on combined probability of 2 noninvasive tests is discussed. Results obtained in hypertensive LV hypertrophy showed a 20% to 30% incidence of abnormal exercise test results, and these positive findings were predictive for the development of typical angina during a 3-year follow-up. Based on these results and reported data, it is extrapolated that patients with silent ischemia may contribute up to 40% of the coronary mortality observed in previous antihypertensive trials. These findings suggest the need for an early detection and separate follow-up of these patients with silent CAD, to better assess the influence of antihypertensive treatment on coronary morbidity and mortality.

Diltiazem prevents hypertrophy progression, preserves systolic function, and normalises myocardial oxygen utilisation in the spontaneously hypertensive rat.

The effects of diltiazem, a calcium channel blocker, and methyldopa, an adrenergic blocker, on left ventricular hypertrophy and left ventricular function were assessed in spontaneously hypertensive rats and Wistar-Kyoto controls. Diltiazem (30 mg.kg-1/day), methyldopa (400 mg.kg-1/day), or placebo were given with water for six months. Left ventricular function was studied in 12 month old animals using an isovolumetrically contracting heart preparation by measuring maximum developed pressure and myocardial oxygen consumption. Systolic blood pressure was reduced by both drugs but more so by methyldopa. Despite its lesser antihypertensive effect, diltiazem reduced heart to body weight ratios in the spontaneously hypertensive rat to a similar degree as methyldopa (3.4(0.2) and 3.4(0.1) compared with placebo 3.7(0.2), p less than 0.05). Maximum developed pressure increased with methyldopa and diltiazem compared with placebo (188(11) and 200(11) vs 166(11) mmHg, p less than 0.05). Myocardial oxygen consumption was lower in the spontaneously hypertensive rat receiving placebo than in the controls (22.8(3.2) vs 28.3(3.8) ml.min-1.100 g-1, p less than 0.05) and was significantly increased by diltiazem but not by methyldopa (27.9(0.4) vs 24.5(0.6) ml.min-1.100 g-1, p less than 0.05 and NS respectively vs the spontaneously hypertensive rat receiving placebo). Diltiazem and methyldopa normalised the isomyosin composition in the spontaneously hypertensive rat. Myocardial concentrations of energy related metabolites obtained at maximum developed pressure were not different between spontaneously hypertensive rats receiving placebo and controls. However, both diltiazem and methyldopa treated spontaneously hypertensive rats showed a significant reduction in adenosine triphosphate and phosphocreatine and a rise in inorganic phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative studies of calcium-channel blockers and beta-blockers in essential hypertension: clinical implications.

The use of calcium-channel blockers to treat essential hypertension is increasing, and in the United States several new drug applications for this indication are under consideration by the Food and Drug Administration. Although the ability of the calcium-channel blockers to lower blood pressure has been established, their efficacy and safety in relation to current therapy require further clarification. This article reviews studies in which calcium-channel blockers and beta-blockers have been compared, including seven with verapamil, four with nifedipine and nitrendipine and two with diltiazem. These studies indicate that the two classes of agents produce similar antihypertensive effects and are associated with a comparable incidence of adverse reactions. In addition, the preliminary findings of a multicenter trial in which 50 subjects with mild or moderate hypertension were treated with diltiazem (60 to 180 mg bid) or propranolol (80 to 240 mg bid) for 4 to 6 months are presented. Both medications significantly lowered blood pressure (from 148 +/- 17/101 +/- 5 to 133 +/- 25/88 +/- 9 mm Hg on diltiazem and from 154 +/- 22/104 +/- 6 to 146 +/- 23/91 +/- 11 mm Hg on propranolol). Fifty-nine percent of the patients on diltiazem and 40% of those on propranolol achieved the treatment goal of a supine diastolic blood pressure under 90 mm Hg together with minimum 10 mm Hg reduction. In a similar study, exercise blood pressure and exercise capacity were also examined, with the most important finding being a reduction in maximal oxygen consumption and exercise duration on propranolol without a significant change on diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)

Diltiazem versus propranolol in essential hypertension: responses of rest and exercise blood pressure and effects on exercise capacity.

Both beta-blocking and calcium channel-blocking drugs are being used with increasing frequency as initial therapy for essential hypertension. The present study was designed to compare the antihypertensive effects of a beta-blocking drug, propranolol, with a calcium channel-blocking drug, diltiazem, at rest and during upright bicycle exercise and to determine whether exercise capacity is altered by these therapies. Twenty-one patients with uncomplicated systemic hypertension and a diastolic blood pressure (BP) of 95 to 110 mm Hg without medication were randomly assigned to propranolol or diltiazem therapy in a double-blind manner. The total daily dosages were titrated as needed, from 160 to 480 mg of propranolol (mean 371 mg) and 120 to 360 mg of diltiazem (mean 307 mg) over 12 weeks, and the titrated dose was maintained for 4 additional weeks. Both drugs significantly reduced supine BP (from 149 +/- 14/101 +/- 4 to 136 +/- 17/89 +/- 10 mm Hg with propranolol and from 157 +/- 14/103 +/- 4 to 144 +/- 13/93 +/- 8 with diltiazem. Only diltiazem reduced BP during submaximal exercise, but both agents produced significant responses during maximal exercise. Diltiazem had no effect on maximal heart rate, exercise duration or O2 uptake, whereas propranolol reduced maximal VO2 from 27 +/- 6 to 22 +/- 6 ml/min/kg (p less than 0.01) and also shortened duration of exercise. Propranolol, despite its effects on heart rate, maintained the workload VO2 relation at submaximal loads, suggesting an increased oxygen delivery. However, these adaptive mechanisms appear to be insufficient during maximal effort.

Comparison and additivity of nitrendipine and hydrochlorothiazide in systemic hypertension.

Calcium channel blockers are highly effective antihypertensive agents and provide a good alternative to other medications used as initial or monotherapy. Although the calcium channel blockers act as peripheral vasodilators, they are unique among this group of drugs in lowering blood pressure in a sustained manner; several compensatory mechanisms are inhibited by virtue of either direct or indirect effects of these agents. In recent years, hypertension has generally been treated with a step-care approach, the limitations of which are now becoming apparent. Today, 4 classes of agents are effective and well tolerated as single therapy and might therefore be considered as first-line drug therapy: diuretics, beta blockers, converting enzyme inhibitors and calcium channel blockers. Preliminary results from an ongoing double-blind randomized trial comparing nitrendipine (a calcium channel blocker) and hydrochlorothiazide (a diuretic) in mild to moderate hypertension will be presented. Results from 63 patients showed the 2 agents to be equivalent in antihypertensive effects and in frequency of adverse reactions. Other data indicate that when nitrendipine and hydrochlorothiazide were combined, a further decrease in blood pressure was observed. Patient characteristics affecting drug choice and clinical situations in which calcium channel blockers can be used most effectively can now often be delineated.

Intertest variability of echocardiographic and chest X-ray measurements: implications for decision making in patients with aortic regurgitation.

Echocardiograms and chest X-ray examinations are commonly employed for serial measurements of left ventricular size and function in patients with chronic aortic insufficiency and often support or even determine therapeutic decisions. This study was undertaken to assess the intertest variability of these measurements made from M-mode echocardiograms and X-ray films performed 3 months apart without intervening clinical or therapeutic changes in 22 patients with significant but asymptomatic aortic insufficiency. End-diastolic and end-systolic dimensions, fractional shortening and cardiothoracic ratios were measured by the same reader, with the initial and 3 month tests being read both independently and together for comparison. The mean values for the initial and 3 month studies were similar, but the intertest variability was substantial, especially when the two tests were read independently. The 95% prediction limits are approximately 50% smaller when the serial studies are read together for comparison. The coefficient of variation for end-diastolic and end-systolic dimensions was 6.1 and 10.1%, respectively, and that for fractional shortening was 17.1%. These findings translate into 95% level prediction limits exceeding +/- 8 mm for left ventricular dimensions and 0.12 for fractional shortening; changes on serial evaluations would have to exceed these values to be considered with a high degree of certainty to represent more than random variability. Although this variability may reflect a number of biologic and technical factors, it emphasizes the need to be cautious in making decisions based solely on changes between two tests, particularly if they are not evaluated together.

Correlates and prognostic implication of exercise capacity in chronic congestive heart failure.

Previous studies have shown poor correlations between exercise tolerance and measurements of left ventricular (LV) function during rest in patients with congestive heart failure (CHF). To further evaluate the determinants of exercise tolerance and their relation to prognosis, we performed rest and exercise hemodynamic measurements and blood pool scintigraphy in 27 patients with CHF. All patients were treated with digitalis and diuretic drugs, but not vasodilator drugs. Exercise capacity was assessed by maximal oxygen consumption (VO2max) during upright bicycle ergometry. Both right ventricular (RV) and LV ejection fractions were measured by radionuclide techniques, and arterial, right atrial and pulmonary artery pressures, cardiac output, and derived hemodynamic indexes were determined. As a group, patients with severely impaired exercise tolerance (group 1, VO2max less than 10 ml/min/kg) had significantly higher rest pulmonary capillary wedge and right atrial pressures (30 +/- 4 vs 23 +/- 6 and 12 +/- 4 vs 7 +/- 2 mm Hg, respectively) than those with a VO2max of 10 to 18 ml/min/kg (group 2). They also had lower LV and RV ejection fractions (16 +/- 4% vs 21 +/- 4% and 19 +/- 12% vs 27 +/- 7%, respectively). However, overlap among individual patients was considerable, and only pulmonary capillary wedge pressure at rest correlated significantly (r = 0.69, p less than 0.001) with VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)