Abnormal recovery systolic blood pressure response for detecting coronary artery disease in men and women investigated by upright bicycle exercise.

We investigated the clinical significance of recovery systolic blood pressure (SBP) ratio, obtained dividing the recovery SBP at 1st (R1/A) or 3rd min (R3/A) by the peak exercise SBP (before stopping), during upright bicycle exercise in 530 subjects (ranging from 17 to 73 years). Our results may be summarized as follows: 1) we found a higher value of R1/A in control subjects with exercise induced ST depression; 2) the normal range in women was higher than in men; 3) the use of recovery SBP ratios gives a lower sensitivity and a higher specificity than ST segment analysis in detection of CAD; 4) this pattern may be useful particularly in patients with previous myocardial infarction and not detectable ST segment analysis during exercise.

Exercise time: a possible source of misleading results during long-term pharmacological studies by multiple stress testings in coronary artery disease.

The assessment of chronic pharmacological treatment of stable angina requires serial exercise stress testings. It is well known that exercise tolerance can be improved by the training effect of performing repeated testings. Our study investigated the values of heart rate, systolic blood pressure, rate-pressure product, and duration of exercise at 0.1 mV ST depression during exercise and the same parameters plus the maximal ST-segment depression at peak exercise, collected from three different tests. The first and second were performed at one-week intervals before, and the third (75 days after the first), was performed after a double-blind study with a drug versus placebo. We found a significant increase of exercise duration at 0.1 mV ST depression and at peak exercise, while 6 of 12 patients increased exercise duration from the second to the third test. Individual variability of exercise duration showed increasing values, ranging from 0 to 71% (first vs. third test). In contrast, the ratio of heart rate and systolic blood pressure did not differ between the tests. Our data criticized the use of mean values of exercise time for pharmacological studies; moreover, individual variability could affect results independently of drug or placebo administration. These findings should be taken into account in order to exclude misleading results.

Atenolol and/or nifedipine in effort angina: which is the treatment of choice for exercise coronary protection?

The authors performed a long-term, double-blind, crossover, randomized study on the effects of two drugs (atenolol, 100 mg/day, or nifedipine, 10 mg t.i.d.) when administered alone or in combination on the exercise tolerance in 10 patients with stable angina on effort (mean age 52 +/- 4 years, 8 males and 2 females) and documented significant (greater than or equal to 70%) obstructive coronary lesions at angiography. None of the drug treatments improved exercise duration or maximal sustained work load. Atenolol decreased significantly ST segment depression to -1 +/- 0.8 from -1.91 +/- 0.7, baseline and -2.05 +/- 0.5, placebo. Nifedipine was not better than placebo. The atenolol plus nifedipine treatment was better than placebo (p less than 0.001) or nifedipine alone (p less than 0.05) but was not more significantly efficacious than atenolol alone. Long-term management of exertional angina can be usefully performed using atenolol. The use of nifedipine at the present dose of 10 mg, although well tolerated, did not improve the ST signs of ischemia.

Long-term management of exercise-induced myocardial ischemia. Diltiazem versus propranolol, a double-blind, crossover study.

The authors performed a long-term, double-blind, crossover study on the effect of two drugs (propranolol, 40 mg t.i.d. or diltiazem, 60 mg t.i.d., each administered for 2 months) on their exercise tolerance in 13 patients with stable angina (mean age 52 +/- 7 years, 9 males and 4 females), after exertion and documented significant (greater than or equal to 70%) obstructive coronary lesions at angiography. Only propranolol, by decreasing heart rate and rate-pressure product, improved maximal sustained work load and duration of exercise (measured by a bicycle ergometer) versus the placebo (p less than 0.05). In both cases, however, they did not find any significant difference between propranolol and diltiazem. ST segment depression was decreased by both drugs (-1.73 +/- 0.95, baseline, vs -0.94 +/- 1.01, propranolol, and -0.95 +/- 0.76, diltiazem, p less than 0.5, for both). Long-term management of stable angina on effort therefore, can be usefully performed using propranolol or diltiazem.

Relation between QT and QS2 intervals during exercise and recovery. Response in patient with coronary artery disease and age-matched control subjects.

We investigated the relationship between QT interval and QS2 (electromechanical systole) during exercise and recovery in patients with coronary artery disease (CAD) and exercise-induced myocardial ischemia (n = 12), and in age-matched controls (n = 20). Upright bicycle exercise was performed (50 watts/min + 20 watts/min every 2 min), recording electrocardiographic lead 2 (100 mm/sec) for QT and QS2 measurement at rest, at each step of uninterrupted exercise and every 60 sec during a 3-min recovery period. Resting data showed a QT less than QS2 finding in both groups; during exercise, QT and QS2 decreased. The values of QT and QS2, collected at each step of exercise and plotted against heart rate (HR) separately for both groups, showed a significant correlation coefficient. Comparing the regression lines of HR-QT and HR-QS2 separately for both groups, we found that both intervals decreased in parallel and the mean QT remained shorter than QS2 in both groups during exercise. The QT/QS2 ratio remained unchanged significantly during exercise and recovery in CAD. In control subjects, the ratio remained unchanged during exercise and the first min of recovery, while a significant change was detected in late (2,3 min) recovery from an adrenergic-induced effect. The mean exercise-induced response of QT-QS2 relationship includes a QT less than QS2 pattern in both groups. In CAD patients, an abnormal pattern was found in two patients during recovery by a relative prolongation of QT, suggesting the possibility of a risk factor for dangerous arrhythmias or sudden death.

Abnormal systolic time intervals in obesity and their relationship with the amount of overweight.

We studied 17 severely obese subjects (age range 26 to 42 years), without hypertension, diabetes mellitus, angina, or clinical signs of heart failure or respiratory disease, and 16 age-matched control subjects. X-teleroentgenographic findings (transverse cardiac diameter and cardiothoracic ratio), blood pressure, and mechanocardiographic parameters were analyzed in both groups. By means of conventional simultaneous recordings of ECG, phonocardiogram, and carotid pulse (100 mm/sec), systolic time intervals were calculated as mean values from 10 beats in the morning. The following comparisons were made by means of analysis of variance: heart rate, preejection period (PEP), rate-corrected PEPI (PEPI), left ventricular ejection time (LVET), and QS2 interval (QS2); the latter two were both corrected for heart rate, respectively, as LVETI and QS2I and the PEP/LVET ratio. Abnormal x-ray data were shown in the obese group along with higher values for heart rate, PEP, PEPI, and PEP/LVET and a shorter LVETI; there were no differences in QS2I or blood pressure. There was a correlation between the amount of overweight and, respectively, transverse cardiac diameter (r = 0.84), heart rate (r = 0.69), PEP (r = 0.49), PEPI (r = 0.59), LVETI (r = -0.61), and PEP/LVET ratio (r = 0.72). A correlation was also found between transverse cardiac diameter and PEP/LVET (r = 0.67). We conclude, therefore, that abnormalities in the mechanocardiographic parameters are related to cardiac enlargement, suggesting a preclinical cardiac dysfunction secondary to chronic cardiocirculatory overload in severe obesity. Thus systolic time intervals appear to be affected by preclinical abnormalities of cardiac performance in these subjects.

Exercise-induced changes of left ventricular ejection time in noninvasive evaluation of chest pain.

Significance and clinical usefulness of exercise-induced changes of noninvasive left ventricular ejection time, recorded by mechanocardiography, in detecting coronary artery disease is still controversial. We investigated the changes of the left ventricular ejection time (LVET), corrected for heart rate as ETI (LVET/square root RR), after a standard 4-min exercise by bicycle ergometer (50 W/min for 2 min, increased by 20 W after 2 min) in 56 male volunteers. They were invasively studied for typical or atypical chest pain. Thirty-four had coronary artery disease (CAD) and the others served as controls. Immediately after exercise LVET shortened according to the rise in heart rate in both groups. ETI increased similarly. After 2 minutes from exercise ETI increased only in the CAD group, according to a longer LVET, in spite of the rise in heart rate. In contrast, ETI was unchanged in controls, according to a shortened LVET. Totally, 27/34 CAD patients and 9/22 controls had a greater ETI than at rest. Employing this delta ETI as a "marker" of CAD we found a predictive accuracy of 74%. We suggest postexercise ETI could be a simple and inexpensive support to electrocardiogram in basic evaluation of subjects with chest pain.

Relation between heart rate and QT interval in exercise-induced myocardial ischemia.

The relation between heart rate and QT interval during dynamic upright exercise on a bicycle ergometer was investigated in control subjects (n = 18) and in patients with coronary artery disease (CAD), stable angina on effort, and angiographically documented significant coronary stenoses (n = 23). Both groups had a significant negative linear relation between heart rate and QT, with a higher correlation coefficient in control subjects (r = -0.78) than in patients with CAD (r = -0.64). This response may be a result of the nonhomogeneous response to ischemia in patients with CAD, particularly with regard to the different impact of exercise-induced ischemia. When the 2 regression lines were compared, a flatter slope was found in the CAD group (p less than 0.001) as a consequence of a faster decrease in the QT-increasing rate in control subjects. It is suggested that in control subjects exercise-induced increase in adrenergic tone causes a rapid and relevant decrease in QT-interval duration. In the CAD group, exercise-induced ischemia relatively prolonged the QT interval; this may have been the result of an impairment of myocardium in response to catecholamines release during exercise or the consequence of a direct effect of exercise-induced ischemia prolonging the duration of myocardial tension.