Comparison of exercise stress testing with ambulatory electrocardiographic monitoring in the detection of myocardial ischemia after unstable angina pectoris.
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Angina, Unstable↗
Biomedical subjects
D T Kelly
Publications and source records attributed to D T Kelly.
Prognostic significance of right ventricular ejection fraction following inferior myocardial infarction.
The prognostic significance of right ventricular ejection fraction, measured by radionuclide ventriculography, was assessed in 168 consecutive patients with inferior myocardial infarction. Right ventricular ejection fraction was 0.40 or less in 35 patients. Over a follow-up period of 40 months, there were 15 deaths in the total group of 168 patients, eight (23%) in the 35 with right ventricular ejection fraction of 0.40 or less, and seven (5%) in the remainder of the group. The one year survival of patients with right ventricular impairment (84 +/- 6%) was significantly worse (P less than 0.01) than those with a right ventricular ejection fraction over 0.40 (95 +/- 2%). A multivariate Cox model analysis showed age (P less than 0.001), left ventricular ejection fraction (P less than 0.01), and right ventricular ejection fraction (P less than 0.03) to be independent predictors of survival. Impaired right ventricular function is an adverse prognostic factor in patients with inferior infarction, particularly in those with impaired left ventricular function.
Female↗
Prognostic significance of a predischarge exercise test in risk stratification after unstable angina pectoris.
The prognostic significance of exercise testing was compared with clinical and electrocardiographic (ECG) variables in a prospective study of 107 patients with unstable angina discharged from the hospital on medical therapy. During a follow-up period of 12.8 +/- 1.4 months, 10 patients (9%) had a nonfatal myocardial infarction (n = 8) or died (n = 2) and 22 (20%) were readmitted with recurrent unstable angina. The relation between 20 clinical, ECG and exercise test variables and the risk of adverse outcome (death, nonfatal myocardial infarction or recurrent unstable angina) was analyzed using both univariate and multivariate (logistic regression) analysis. Univariate predictors of adverse outcome included diabetes mellitus, evolutionary T wave changes, T wave changes on the preexercise ECG and low maximal rate-pressure product during exercise. Independent predictors of adverse outcome in multivariate analysis included diabetes mellitus, evolutionary T wave changes after admission, rest pain during hospitalization, ST depression during exercise and low maximal rate-pressure product. A predictive model constructed using the regression equation and all independent predictors stratified patients into high and low risk groups (41% and 5% risk of adverse outcome, respectively). The result of a predischarge exercise test adds independent prognostic information to clinical and ECG data in medically treated patients with unstable angina and could be used in combination with clinical and ECG data to identify patients at risk of adverse events.
Angina, Unstable↗
Clinical significance of silent ischemia in unstable angina pectoris.
In a prospective study the significance of silent ischemia was evaluated in 66 patients with a clinical diagnosis of unstable angina (no requirement for reversible ST-T changes during pain on 12-lead electrocardiograms before entry), and the results of continuous 2-channel electrocardiographic (ECG) recordings, begun within 24 hours of admission, were compared with other clinical and ECG predictors of adverse outcome. Ischemic changes were detected in 7 patients (11%) during a mean of 41 hours of recording. There were 37 episodes of transient ST-segment change (16 ST elevation, 21 ST depression) of which 11 (30%) were symptomatic and 26 (70%) were silent. All 7 patients had at least 1 silent episode and 5 also had symptomatic episodes during the recording but only 2 patients had exclusively silent episodes. During a mean follow-up of 13.3 months, 3 patients died, 5 had a nonfatal myocardial infarction and 32 required revascularization. Although transient myocardial ischemia during the continuous ECG recording, whether silent or symptomatic, was a specific predictor of subsequent nonfatal myocardial infarction or death (specificity 92%), its sensitivity for these events was low (25%). In contrast, recurrent rest pain (greater than or equal to 1 episode) occurred in all patients with these serious adverse events (sensitivity 100%, specificity 49%). Transient ischemia occurs infrequently during continuous ECG recordings in patients with unstable angina not selected by reversible ST-T changes on a 12-lead electrocardiogram at entry. Recurrent rest pain after hospital admission is a more sensitive predictor of serious events in this group.
Angina Pectoris↗
Effects of verapamil on the anaerobic threshold and peak oxygen consumption in effort angina pectoris.
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Adult↗
Effects of diltiazem and long-term beta 1-adrenergic blockade on hemodynamics and blood flow during exercise in patients with stable angina pectoris.
The short-term effects of oral diltiazem on hemodynamics and distribution of cardiac output at rest and during semiupright bicycle exercise were evaluated in eight patients with stable effort angina on long-term beta 1-adrenergic blockade. Cardiac output and iliofemoral blood flow were measured using thermodilution. The patients were exercised to the same work load on a bicycle before and 2 h after oral diltiazem (60 mg in two patients and 120 mg in six). At maximal exercise, diltiazem reduced heart rate from 94 +/- 5 to 88 +/- 6 beats/min (p less than 0.01), mean arterial pressure from 139 +/- 5 to 127 +/- 4 mm Hg (p less than 0.01) and systemic vascular resistance from 9.7 +/- 0.7 to 8.4 +/- 0.4 x 10(2) dynes.s.cm-5 (p less than 0.05) compared with control. During exercise, cardiac output, iliofemoral blood flow, mean pulmonary wedge pressure and mean right atrial pressure were not altered, but stroke volume increased from 119 +/- 11 to 131 +/- 10 ml (p less than 0.05). Maximal ST segment depression during exercise was decreased and angina was less. Diltiazem does not alter the distribution of the cardiac output during exercise but improves ischemia.
Adrenergic beta-Antagonists↗
Hemodynamic and metabolic basis of impaired exercise tolerance in patients with severe left ventricular dysfunction.
Hemodynamic and metabolic changes were measured at rest and during exercise in 23 patients with chronic heart failure and in 6 control subjects. Exercise was limited by leg fatigue in both groups and capacity was 40% lower in the patients with failure. At rest, comparing patients with control subjects, heart rate and right atrial and pulmonary wedge pressure were higher; cardiac output, stroke volume and work indexes and ejection fraction were lower; mean arterial and right atrial pressure and systemic resistance were similar. During all phases of exercise in patients with heart failure, pulmonary wedge pressure and systemic vascular resistance were higher and pulmonary vascular resistance remained markedly elevated compared with values in control subjects. Cardiac output was lower in the patients with failure, but appeared to have the same physiologic distribution in both groups during exercise. Although arterial-femoral venous oxygen content difference was higher in patients with heart failure, this increase did not compensate for the reduced blood flow. Even though the maximal oxygen consumption was significantly reduced, femoral venous lactate and pH values were higher than values in control subjects, but femoral venous pH was similar in both groups at their respective levels of maximal exercise. Ejection fraction was lower in those with heart failure at rest and did not increase with exercise. Ventilation in relation to oxygen consumption was higher in patients with failure than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Heart failure--management in the 1990s.
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Clinical Protocols↗
Risk of adverse outcome in patients admitted to the coronary care unit with suspected unstable angina pectoris.
One hundred ninety-six consecutive patients admitted to the coronary care unit with suspected unstable angina were classified clinically as having either definite (113 patients) or suspected unstable angina (83 patients) within 24 hours of admission. Patients were followed prospectively to determine their outcome in the hospital and in the first 4 months after discharge. Three patients had a non-fatal myocardial infarction in the hospital and 2 died (1 fatal myocardial infarction, 1 death immediately after coronary bypass surgery). During follow-up (mean 4.2 +/- 2.3 months), 6 additional patients had a nonfatal myocardial infarction, 4 died and 22 were readmitted with definite unstable angina. The incidence of nonfatal infarction or death was significantly lower in patients with suspected unstable angina during both the primary hospital admission (0 of 83 vs 5 of 113, p less than 0.05) and after discharge from the hospital (1 of 83 vs 9 of 113, p less than 0.05), and fewer patients with suspected unstable angina were readmitted with a recurrence of definite unstable angina (1 of 83 vs 21 of 113, p less than 0.001). Thus, a simple clinical classification into definite or suspected unstable angina performed within 24 hours of admission to the coronary care unit identified a substantial group with a low short-term risk of adverse events.
Aged↗
Evaluation of a microprocessor-controlled sphygmomanometer for recording blood pressure during exercise.
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Adult↗
Exercise stress-induced changes in systemic arterial potassium in angina pectoris.
Large fluctuations in systemic arterial potassium have been found during and after exercise in normal subjects. To determine whether similar changes occur in patients with angina pectoris, arterial potassium levels were measured before, during and immediately after maximal bicycle exercise in 20 patients with exertional angina. In 10 of these patients, leg blood flow and arteriovenous potassium levels also were measured. During exercise, arterial potassium increased significantly both from rest to submaximal exercise (4.3 +/- 0.1 to 4.7 +/- 0.1 mmol/liter, p less than 0.01) and from submaximal to maximal exercise (5.4 +/- 0.1 mmol/liter, p less than 0.01). Within 1 minute of cessation of exercise, arterial potassium had decreased to 4.7 +/- 0.1 mmol/liter (p less than 0.001) and continued to decrease to a minimum of 4.1 +/- 0.1 mmol/liter between 3 and 5 minutes after exercise, significantly less than the rest value (p less than 0.05). At maximal exercise (99 +/- 9 watts), the calculated release of potassium from each leg reached 2.7 +/- 1.3 mmol/min. Four minutes after exercise, the leg muscles were resorbing potassium at 0.24 mmol/min. In these patients with exertional myocardial ischemia, the magnitude and rapidity of arterial potassium changes during and after exercise resemble those found in normal subjects, but occurred at much lower workloads. Release and resorption of potassium by exercising muscle in patients with angina pectoris may cause potentially arrhythmogenic arterial potassium fluctuations.
Adult↗
Effects of nisoldipine on systemic and leg blood flow, oxygen transport and metabolism, and hemodynamics during exercise in effort angina pectoris.
The acute effects of 10 mg of oral nisoldipine on hemodynamics, oxygen transport and metabolism, and distribution of cardiac output, at rest and during semiupright bicycle exercise, were evaluated in 10 men with effort angina receiving long-term beta 1 blockade. Cardiac output and leg blood flow were measured using the thermodilution technique. At rest, nisoldipine decreased systemic resistance from 18.9 +/- 1.0 to 15.9 +/- 1.2 dynes.s.cm-5.10(2) (p less than 0.05) and cardiac output increased from 4.8 +/- 0.2 to 5.3 +/- 0.3 liters/min (p less than 0.05) without changing leg blood flow. During maximal exercise with nisoldipine, systemic resistance was reduced (10.6 +/- 0.9 to 8.6 +/- 0.5 dynes.s.cm-5.10(2), p less than 0.05) and cardiac output increased 18% (10.3 +/- 0.7 to 12.2 +/- 0.6 liters/min, p less than 0.05) when compared with control values. Exercise heart rate was higher with nisoldipine (113 +/- 4 vs 106 +/- 4 beats/min, p less than 0.01), but the mean arterial pressure was not significantly changed, giving a higher rate-pressure product. The increase in mean pulmonary artery wedge pressure was attenuated (26 +/- 3 vs 30 +/- 3 mm Hg during control exercise, p less than 0.05), but ST depression was unaltered. Exercise leg flow was reduced by nisoldipine from 4.3 +/- 0.4 to 3.9 +/- 0.3 liters/min (p = 0.07) and the proportion of cardiac output distributed to the legs was reduced from 42 +/- 3 to 33 +/- 3% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Comparison of the effects of nifedipine and nitroglycerin on hemodynamic determinants of myocardial oxygen consumption and supply during exertional angina.
To investigate the antianginal action of nitroglycerin and nifedipine, systemic and right heart pressures, cardiac output, oxygen consumption, and radionuclide left ventricular ejection fraction and volume were measured in 14 men with stable effort angina and a positive exercise electrocardiogram. Exercise tests were performed on a semiupright bicycle ergometer on no therapy and after intravenous nitroglycerin and sublingual nifedipine, which lowered mean arterial pressure by 20 mm Hg. Exercise tolerance improved from 50 +/- 4 to 61 +/- 5 W on nifedipine and to 79 +/- 4 W on nitroglycerin (p less than 0.01, nitroglycerin vs. nifedipine). At submaximal workloads, both drugs decreased arterial pressure and ventricular volumes, but heart rate was higher on nifedipine. At peak exercise on nitroglycerin (79 W), oxygen consumption, cardiac index, heart rate, and rate-pressure product were significantly increased over peak control and nifedipine values, while systolic pressure and end-diastolic volume were unchanged. Nitroglycerin reduced pulmonary wedge pressure more and systemic diastolic pressure less than nifedipine, so the coronary perfusion gradient was reduced by nifedipine and maintained by nitroglycerin. Also, there was less angina and ST-segment depression after nitroglycerin compared to control or nifedipine, and the left ventricular diastolic pressure-volume relationship was improved only by nitroglycerin. This suggests that the action of nitroglycerin in reducing ischemia is not only due to reduced myocardial oxygen demand, but that myocardial oxygen delivery may also be increased.
Adult↗
Multiple action compounds in angina pectoris.
Carvedilol--a vasodilating beta-blocker has been shown in multicentre trials to be as effective as standard beta-blockers in improving exercise tolerance in patients with angina pectoris and it is more effective than nifedipine. The side effects are less than conventional beta-blockers and nifedipine. Carvedilol is an effective anti-anginal therapy and improves the quality of life.
Adrenergic beta-Antagonists↗
Regional distribution of cardiac output at rest and during exercise in patients with exertional angina pectoris before and after nifedipine therapy.
The short-term effects of sublingual nifedipine (20 mg) on cardiac output and its distribution at rest and during exercise were evaluated by measurement of iliofemoral blood flow and cardiac output in 10 men with stable angina pectoris controlled by metoprolol. At rest, nifedipine significantly decreased iliofemoral vascular resistance from 294 +/- 36 to 165 +/- 29 dynes.s.cm-5.10(2) (p less than 0.01) and significantly increased iliofemoral blood flow from 0.34 +/- 0.04 to 0.57 +/- 0.11 liters/min (p less than 0.05). Systemic vascular resistance was reduced from 19 +/- 1 to 13 +/- 1 dynes.s.cm-5.10(2) (p less than 0.001) and cardiac output increased significantly from 4.7 +/- 0.3 to 5.8 +/- 0.5 liters/min (p less than 0.05). Mean arterial pressure decreased significantly and heart rate increased significantly. During maximal upright bicycle exercise during nifedipine therapy, iliofemoral vascular resistance and leg blood flow were unchanged compared with control (23 +/- 2 versus 21 +/- 3 dynes.s.cm-5.10(2) and 4.7 +/- 0.5 versus 4.4 +/- 0.6 liters/min), cardiac output remained significantly increased (12.8 +/- 0.8 to 15.2 +/- 1.2 liters/min, p less than 0.05) and systemic vascular resistance remained significantly reduced (8 +/- 1 to 5 +/- 1 dynes.s.cm-5.10(2); p less than 0.001). The proportion of cardiac output distributed to the working lower limbs was significantly reduced at all exercise levels. In summary, nifedipine caused a redistribution of cardiac output by vasodilating nonexercising vascular beds without altering the locally mediated vasodilation in exercising muscle. In patients with coronary artery disease given nifedipine therapy, an increase in exercise tolerance is due to relief of myocardial ischemia rather than to increased peripheral oxygen delivery.
Adult↗
Antianginal effects of nitroglycerin during exercise-induced angina: hemodynamic and left ventricular function changes related to indexes of myocardial oxygen consumption.
In 14 patients during exercise, intravenous nitroglycerin improved anginal threshold and increased workload compared with control subjects. At similar workloads, the decreased left ventricular volumes suggested decreased myocardial oxygen consumption due to peripheral unloading. At maximal exercise with nitroglycerin (50 +/- 17 to 79 +/- 15 watts), rate-pressure product and end-diastolic volumes were higher with less ischemia, suggesting myocardial supply was improved by nitroglycerin.
Angina Pectoris↗
Comparison of carvedilol and atenolol for angina pectoris.
The antianginal efficacy of carvedilol, a novel beta-blocking agent with vasodilating action, and atenolol were compared in 12 patients with stable effort angina and a positive stress test response. All patients received single doses of placebo, carvedilol, 25 and 50 mg, and atenolol, 50 mg. Heart rate at rest was reduced by 11 and 12 beats/min with both drugs, but only carvedilol, 50 mg, reduced blood pressure at rest. Both carvedilol, 50 mg, and atenolol, 50 mg, increased mean exercise time (24% and 34%, respectively, compared with placebo), time to angina (35% and 51%, respectively), and time to 1 mm of ST-segment depression (54% and 102%, respectively, p less than 0.05 carvedilol vs atenolol). Carvedilol, 25 mg, produced smaller, directionally similar changes in exercise performance, which did not reach statistical significance except for time to 1 mm of ST depression. Both drugs in the 50-mg dose reduced ST-segment depression similarly at maximal and submaximal work levels and lowered heart rate and rate-pressure product at maximal and submaximal work. Carvedilol, 50 mg alone, significantly lowered maximal systolic pressure and rate-pressure product at 1 mm of ST-segment depression. Despite some evidence of vasodilator activity for carvedilol, there was no significant difference in antianginal efficacy with a conventional beta-blocking drug.
Adrenergic beta-Antagonists↗
Validation of a real-time electrocardiographic monitor for detection of myocardial ischemia secondary to coronary artery disease.
A new real-time electrocardiographic (ECG) monitor (QMED Monitor OneTM) was evaluated to assess its accuracy in detecting ischemic ST-segment changes in 43 patients (34 men, 9 women, mean age 56 +/- 11 years) during exercise stress testing. The output of QMED was compared with ST-segment measurements from a Marquette CASE-II computer (ECGM) using a bipolar lead CM5, defining a positive ECG as at least 1 mm of planar or downsloping ST depression. Results were concordant in 33 patients, 15 with both positive and 18 both negative responses, yielding an accuracy (expressed as sensitivity, specificity, positive and negative predictive accuracy) of 83%, 72%, 68% and 86%, respectively. Seven false-positive QMED episodes occurred: 4 due to excess baseline wander or noise in the control ECG, which may have been prevented by reapplication of electrodes, and all 7 episodes were correctly discounted by inspection of the sample ischemic ECG output, yielding an accuracy of 81%, 100%, 100% and 85%. Mean duration and maximal magnitude of ST depression in patients with a positive ECG response was 7.9 +/- 7 minutes and 1.7 +/- 0.6 mm for QMED and 8.9 +/- 7 minutes and 2.2 +/- 0.7 mm for ECGM. The 3 false-negative QMED events were relatively brief and mild ischemic episodes and slight differences in electrode placement between the 2 systems may account for this discrepancy in 2 of the patients. Real-time ST monitoring with QMED is sufficiently reliable for clinical use. Optimal specificity depends on the ability to inspect sample ECG traces to verify a stable baseline and confirm episodes of ischemic ST-segment shift.
Coronary Disease↗