Early and long-term results of coronary artery bypass grafting with severely depressed left ventricular performance

The effects of coronary artery bypass grafting (CABG) on ventricular performance and long-term clinical status were studied in 18 consecutive patients with disabling angina pectoris and severely depressed left ventricular (LV) performance (ejection fraction [EF] 27 +/- 9%). All patients survived CABG, although 1 patient had a perioperative myocardial infarction. There was no change in LVEF at rest, 29 +/- 12%, in the other 17 patients. However, LVEF during peak exercise increased from 22 +/- 7% to 27 +/- 14% (p less than 0.05). The 17 patients were separated into 2 groups: those who increased their peak exercise LVEF by at least 10% (group A, 8 patients) and those who increased it by less than 10% (group B, 9 patients). Preoperatively, patients in group A had a higher LVEF at rest (p less than 0.001) and smaller end-systolic and end-diastolic volumes at rest (p less than 0.001) and during exercise (p less than 0.005). Preoperatively, the LVEF in group A decreased with exercise, from 36 +/- 4% to 27 +/- 5% (p less than 0.01), but was unchanged in group B (19 +/- 3% vs 17 +/- 4%, difference not significant). After CABG, patients in group A had a smaller increase in end-systolic volume with exercise than those in group B (13 +/- 7 vs 34 +/- 22 ml/m2, p less than 0.05), but the changes in end-diastolic volume with exercise were not significantly different. At 27 +/- 5 months after CABG, 5 of 8 patients in group A were asymptomatic.(ABSTRACT TRUNCATED AT 250 WORDS)     

Resting and exercise left ventricular function in patients with hypertrophic cardiomyopathy

Left ventricular ejection fraction (EF) at rest and during exercise was measured in 19 patients with hypertrophic cardiomyopathy (HCM) by means of radionuclide angiography. The results were compared to those in 20 normal subjects. Based on hemodynamic data, patients with HCM were divided into three groups. In group I, no demonstrable left ventricular outflow obstruction, there were five patients; their mean EF increased from 68% +/- 8.9 (+/- SD) at rest to 74% +/- 9.2 during exercise (p less than 0.05). In group II, latent obstruction, there were six patients; their mean EF at rest (75.2% +/- 8.2) and at peak exercise (78.7% +/- 6.7) was not statistically different (p greater than 0.05). Group III, obstruction present at rest, consisted of eight patients; EF at rest (82.6% +/- 8.5) decreased significantly during exercise (75.6% +/- 7.7, p less than 0.01). In normal subjects resting EF was 66.3% +/- 7.6; it increased to 76.4% +/- 7 (p less than 0.001). Exercise duration and heart rate-blood pressure product were lower in groups II and III. Thus there are significant differences in left ventricular systolic function both at rest and during exercise between these three major hemodynamic subgroups. These findings emphasize the importance of such a hemodynamic classification of HCM.     

Improvement in exercise capacity and associated changes in hemodynamics and left ventricular function after the addition of metoprolol to nifedipine in patients with stable exertional angina

In 10 men with stable exertional angina, the changes in exercise capacity, hemodynamics, and left ventricular (LV) function were measured after 20 mg sublingual nifedipine (N) and again after adding 100 mg oral metoprolol (M). Nifedipine alone did not significantly improve exercise workloads (+18%) and duration (+21%), but the addition of metoprolol increased both parameters by a further 37 and 32%, respectively (both p less than 0.005 vs. N). After nifedipine the onset of angina was slightly delayed (5.14 +/- 2.41 min placebo (P), 6.00 +/- 2.31 min N, p less than 0.1) and occurred at higher workloads (36 +/- 17 W P, 43 +/- 8 W N, p less than 0.1). After the addition of metoprolol, the onset of angina was delayed substantially more (9.57 +/- 2.22 min, p less than 0.001 vs. P and N) and occurred at much higher workloads (62 +/- 20 W, p less than 0.001 vs. P and N). At rest (R) and during exercise (E), nifedipine decreased systemic vascular resistance (-36% R, -27% E, both p less than 0.001) and mean arterial pressure (-18% R, -21% E, both p less than 0.001), and increased heart rate (+15% R, +11% E, both p less than 0.001), Pulmonary artery wedge pressure on exercise increased less (22 +/- 7 mmHg P, 13 +/- 5 mmHg N, p less than 0.001). After adding metoprolol, the major change was a reduced heart rate (-25% vs. N at R and E, both p less than 0.001), and arterial pressure was unaltered. Pulmonary artery wedge pressure on exercise increased to 18 +/- 5 mmHg (p less than 0.05 vs. N). Exercise LV ejection fraction and volume did not change significantly after adding metoprolol despite marked improvement in angina. In this acute exercise study in patients with stable exertional angina, metoprolol added to nifedipine markedly improved exercise capacity by preventing the increase in heart rate seen with nifedipine. In our patients with relatively normal LV function at rest, the combination was safe and produced no deleterious effects on LV function.     

Effect of captopril on myocardial ischemia, intracardiac hemodynamics and regional left-ventricular contractility in patients with stenocardia]

Technetium-99m pertechnetate equilibrium ventriculography was used to evaluate the effects of captopril in a single dose of 50 mg on the changes in ST segment depression during the identical bicycle ergometer exercise, as well as on systemic and regional hemodynamic parameters in 10 patients (mean age 52 years) with Functional Classes II-III exercise-induced angina pectoris. During exercise performed 45 and 90 minutes after captopril, ST segment depression decreased by 30 +/- 0 (p less than 0.05), and 32 +/- 10% (p less than 0.02), respectively as compared to baseline ST segment displacement. Following 90 minutes after the drug administration, end-systolic volume reduced both at rest and during exercise, resting stroke volume increased from 71 +/- 4 to 76 +/- 4 ml (p less than 0.01), whereas exercise stroke volume rose from 69 +/- 3 to 74 +/- 3 ml (p less than 0.03); with the drug, ejection fraction showed a 5% increase (p less than 0.02) at rest and a 4% increase (p less than 0.02) on exercise. Thus, captopril had a beneficial effect on the hemodynamics and reduced myocardial ischemia in patients with exercise induced angina.     

Left ventricular volume and ejection fraction response to exercise in aortic regurgitation

To test the hypothesis that left ventricular (LV) performance in aortic regurgitation (AR) can be more completely characterized by measurement of LV volumes in addition to ejection fraction (EF), 27 asymptomatic patients (Group 1), and 22 symptomatic patients (Group 2), and 10 control subjects were studied at rest and during upright bicycle exercise using the first-pass technique and a multicrystal scintillation camera. LV end-diastolic volume was measured by the area-length method. In the control group end-diastolic volume increased 14%, end-systolic volume decreased 22%, and EF increased 22% with exercise. In contrast, in Group 1 patients with AR, end-diastolic volume was elevated at rest and during exercise. The 18% decrease in end-diastolic volume during exercise was significantly different from the control response (p less than 0.01). End-systolic volume was also elevated at rest and during exercise, but the 30% decrease during exercise was a response not significantly different from the control. Although mean EF increased 15% in these patients, EF at peak exercise was significantly lower than that in the controls. In Group 2 patients with AR, resting EF was reduced, the EF response to exercise was abnormal, and end-diastolic and end-systolic volume responses to exercise were significantly different from those in Group 1: end-diastolic volume did not change and end-systolic volume increased. In contrast to the fairly uniform volume responses among all Group 1 patients, there were 2 subgroups based on volume changes within Group 2: 7 of 22 had a decrease in end-diastolic volume and end-systolic volume during exercise and 8 of 22 showed an increase in end-diastolic and end-systolic volume during exercise. In conclusion, LV volumes at rest and exercise give more information about LV functional reserve in symptomatic patients with AR than do EF responses alone, and may be useful in separating symptomatic patients who show a normal end-systolic volume response to exercise from those in whom worsening failure develops during exercise.     

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.     

Myocardial ischemia during daily activities: the importance of increased myocardial oxygen demand

The role of increased myocardial oxygen demand in the pathophysiology of myocardial ischemia occurring during daily activities was evaluated in 50 patients with coronary artery disease and exercise-induced ST segment depression. Each patient underwent ambulatory electrocardiographic (ECG) monitoring for ST segment shifts during normal daily activities and symptom-limited bicycle exercise testing with continuous ECG monitoring. All 50 patients had ST depression greater than or equal to 0.1 mV during exercise. A total of 241 episodes of ST depression were noted in the ambulatory setting in 31 patients; only 6% of these were accompanied by angina pectoris. Significant (0.1 mV) ST depression during ambulatory monitoring was preceded by a mean increase in heart rate of 27 +/- 12 beats/min. Patients with ischemia during daily activities developed ST depression earlier during exercise (7.9 +/- 4.4 vs. 14.2 +/- 6.4 min, p less than 0.001) and tended to have significant ECG changes at a lower exercise heart rate and rate-pressure product than did those without ST depression during ambulatory monitoring. In the 31 patients with ischemia during daily activities, the mean heart rate associated with ST depression in the ambulatory setting was closely correlated with the heart rate precipitating ECG changes during exercise testing (r = 0.74, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise two-dimensional echocardiography for diagnosis of coronary artery disease

To improve ultrasound images during exercise 2-dimensional echocardiography (2-D echo), a device was developed to hold the transducer and maintain its orientation relative to the heart. The value of this technique in detecting wall motion abnormalities and changes in ejection fraction was evaluated in 54 men undergoing stress test for angina. Thallium-201 scanning, electrocardiography and exercise 2-D echo were recorded concurrently. Technically satisfactory echo studies were obtained in 47 patients (87%). The sensitivity and specificity of exercise echo in the detection of myocardial ischemia as judged by wall motion abnormalities were 100% and 93%, respectively. Sixteen patients with normal thallium scans increased their ejection fraction (EF) estimated by echo (from 52 +/- 1% at rest to 67 +/- 1% at maximal exercise, p less than 0.001); all showed an increase of 5% or more. In contrast, 11 patients who had reversible thallium scan defects showed a consistent decrease in EF (from 53 +/- 2% at rest to 43 +/- 2% during exercise, p less than 0.001); 20 patients with irreversible thallium scan defects showed no specific trend in the EF (48 +/- 2% at rest and 50 +/- 2% during exercise, difference not significant). Changes in heart rate and blood pressure did not distinguish the 3 groups of patients. Our technique of exercise 2-D echo may be useful for detecting wall motion abnormalities and EF changes during exercise and possibly enhance the sensitivity of thallium scanning in the noninvasive diagnosis of coronary artery disease.     

Clinical and angiographic findings in angina at rest

The purpose of this study was to delineate the clinical, ECG, and angiographic features of a large series of consecutive patients with angina at rest. Transient ST segment elevation during pain was observed in 219 patients (group I), while 220 patients showed ST segment depression during pain (group II). Group II patients were found to have higher incidence of hypertension (p less than 0.001), prior myocardial infarction (p less than 0.0005), history of exertional angina (p less than 0.0005), and a progressive aggravation of symptoms before hospitalization (p less than 0.0005), while group I patients had a prevalence of recent onset angina (p less than 0.05) and more frequently developed severe ventricular arrhythmias during pain (p less than 0.0005). Furthermore, a larger number of patients showing ST segment depression during chest pain had multivessel disease (p less than 0.0005), left main involvement (p less than 0.005), and lower values of left ventricular ejection fraction (p less than 0.001) than patients with ST segment elevation during pain. Survival curves of medically treated patients showed a significantly better long-term prognosis in patients of group I (p less than 0.01). The direction of the ST segment shift during anginal attacks at rest may therefore allow a classification of patients included into the broad spectrum of unstable angina. This distinction should be taken into consideration in studies aimed at evaluating long-term prognosis or the results of medical and surgical therapy.     

Role of myocardial scintigraphy with thallium-201 in the characterization of episodes of transient ischemia at rest. Clinical and electrocardiographic correlates

In the past ten years we studied 80 patients with angina at rest by 201-Thallium perfusion scintigraphy. According to ECG changes during episodes of transient ischemia at rest, the patients were divided into three groups. Thirty six patients showed transient ST segment elevation (Group 1); 33 ST segment depression (Group 2) and 11 normalization of negative T waves (Group 3). 201-TI scintigraphy was performed during spontaneous or ergonovine induced episodes of ischemia and at redistribution. Group 1 showed localized and severe perfusion defects, well correlated to the site of ECG changes. Group 2 showed more diffuse and less severe perfusion defects, less correlated to the site of ECG changes. Group 3 showed perfusion defects similar to those observed in Group 1 and associated in 54% with basal perfusion defects due to previous myocardial infarction. In conclusion: A) three main perfusion patterns are associated with the three types of ECG changes; B) relative to ECG, myocardial scintigraphy provides a more accurate definition of the site and extension of ischemia, particularly in Group 2 patients.     

Verapamil therapy for stable exertional angina pectoris

Clinical and exercise responses to therapy with the calcium-channel blocking agent verapamil were assessed in 26 patients with stable exertional angina pectoris using a double-blind, placebo-controlled, randomized crossover study design. Verapamil, 480 mg daily, reduced the frequency of angina attacks (5.6 +/- 7.3 to 2.2 +/- 3.0 attacks per week, p less than 0.001) and number of nitroglycerin tablets consumed (3.4 +/- 4.9 to 1.2 +/- 2.5 tablets per week, p less than 0.05), and increased exercise duration (6.4 +/- 2.1 to 7.5 to 1.8 minutes, p less than 0.001) (all data are mean +/- standard deviation). These changes were significantly better than those seen with placebo. These beneficial effects of verapamil were related to significant reduction in the heart rate-systolic blood pressure product during submaximal exercise. Adverse effects from verapamil were few and consisted primarily of constipation in 6 patients. A total of 193 patients had been entered in 6 independent clinical trials, which have compared verapamil with placebo for the treatment of stable exertional angina pectoris, using a similar study design. The combined evidence from all these studies indicates that verapamil is a highly effective and safe drug for the treatment of stable effort-related angina pectoris.     

Long-term efficacy of high-dose diltiazem for chronic stable angina pectoris: 16-month serial studies with placebo controls

In order to assess the long-term efficacy of diltiazem for the treatment of angina pectoris, eight patients with chronic stable exertional angina who were previously entered into a 4-month randomized, double-blind placebo controlled study, were studied for an additional 12-months. The patients continued to take diltiazem, 360 mg/day, and underwent treadmill exercise testing after 10 and 16 months of therapy. A single-blind placebo week was introduced after 16 months and a treadmill test was performed at the end of this week. Diltiazem therapy continued to augment exercise duration until 0.1 mV of ECG ST depression at 10 and 16 months as compared to the final placebo period: 573 +/- 133 (SD) seconds at 10 months; 565 +/- 148 seconds at 16 months; vs 431 +/- 151 seconds at final placebo (both p less than 0.001). Also, the time to angina pectoris was prolonged on diltiazem by 181 seconds at 16 months (p less than 0.01) and the total duration of exercise was increased by 101 seconds (p less than 0.001) as compared to placebo. In addition, angina frequency decreased from 17 +/- 11 attacks/week on placebo to 0.6 +/- 0.6 attacks/week during diltiazem therapy at 16 months. Two of the eight patients noted mild pedal edema, but no other adverse effects were experienced. Thus diltiazem, 360 mg/day, can be an effective single agent for the long-term treatment of chronic stable angina pectoris.     

The electrocardiogram and coronary artery spasm

This discussion does not attempt to explain why the ECG of patients during rest angina accompanied by coronary spasm sometimes demonstrates ST segment elevation, at other times less impressive changes and, on occasion, no important change. Regardless, the important point is that ECG changes during an episode of chest pain are not a necessary criterion for the diagnosis of angina pectoris either in patients presenting with rest or exertional chest pain syndromes.     

Correlation of the exercise ST/HR slope with anatomic and radionuclide cineangiographic findings in stable angina pectoris

A rate-related change in ST-segment depression with exercise (ST/HR slope) of 6.0 microV/beat/min or more has been proposed as an accurate predictor of 3-vessel coronary artery disease (CAD). To further assess the accuracy and functional correlates of this method, exercise electrocardiograms were compared with radionuclide rest and exercise left ventricular (LV) ejection fraction (EF) and angiography in 35 patients with stable angina. The ST/HR slope was significantly increased in patients with 3-vessel CAD. An ST/HR slope of 6.0 or more identified 3-vessel CAD with a sensitivity of 89% and specificity of 88%. The predictive value for 3-vessel CAD was 73% owing to the presence of 3 false-positive slopes. The patients from whom these slopes were derived had functionally severe 2-vessel CAD, with an average decrease in exercise LVEF of 13%. Two of these 3 had additional left main CAD and the third has unsuspected additional aortic regurgitation. For the entire group, the exercise ST/HR slope was linearly related to the exercise change in LVEF (r = -0.55, p less than 0.001). Mean exercise change in LVEF for stable angina patients with ST/HR slopes of 4.5 or more was significantly different from that for patients with lower ST/HR slopes (-12 +/- 1% vs + 2 +/- 2%, p less than 0.0001). Thus, the ST/HR slope is both sensitive and specific for the identification of 3-vessel CAD, and high ST/HR slopes in patients with less extensive anatomic disease may predict functionally severe ischemia.     

Noninvasive assessment of left ventricular performance following transluminal coronary angioplasty

We studied 36 patients with successful transluminal coronary angioplasty (group 1) noninvasively using exercise electrocardiography, exercise T1-201 myocardial scintigraphy and equilibrium radionuclide ventriculography before and 3-5 days after the procedure. Six patients who underwent aortocoronary-bypass surgery (group 2) and 10 patients with stable angina pectoris (group 3) served as controls. All patients had arteriographically documented coronary artery disease at least in one major coronary vessel (stenosis greater than or equal to 70%). In group 1, average coronary stenosis was 81.1 +/- 8.4% before dilatation and 44 +/- 13.7% after the procedure (P less than 0.001). Ischemia score in the exercise electrocardiography decreased from 2.4 +/- 2.7 before dilatation to 0.4 +/- 0.8 after the procedure (P less than 0.001). Myocardial perfusion in computerized T1-201 myocardial scintigraphy 5-10 min after exercise expressed as vitality index (the ratio of T1-201 uptake in the ischemic region to the region of maximal uptake in the same image analyzed carefully in the same view in 2 studies) increased from 72.9 +/- 8.4% before dilatation to 79.9 +/- 11.7% after the procedure (P less than 0.001). Ejection fraction at rest increased from 47.2 +/- 9.2% to 51.0 +/- 9.7% (P less than 0.001) and during exercise from 39.9 +/- 10.5% to 49.4 +/- 10.9% (P less than 0.001) before and after the procedure. In group 2, noninvasive studies showed a tendency to improvement after surgery. In group 3 no significant changes were noted. We conclude that transluminal coronary angioplasty improves both coronary perfusion to ischemic areas supplied by critical coronary artery stenoses and left ventricular function, especially during exercise, if luminal diameter is dilated by greater than 20%.     

Significance of hyperventilation-induced ST segment depression in patients with coronary artery disease

To investigate the significance of hyperventilation-induced ST segment depression, 329 consecutive patients with angina and documented coronary artery disease who underwent hyperventilation and exercise tests during pharmacologic washout were studied. The hyperventilation test induced ST segment depression in 79 patients. In 36 of these 79 patients, the electrocardiographic changes occurred early during overbreathing (Group I), whereas in 26 they occurred late during recovery (Group II). Seventeen patients developed ST segment depression both during over-breathing and during recovery (Group III). Group I patients had a higher frequency of history of angina during exercise, multivessel disease and lower tolerance to exercise as compared with patients in Group II. In Group I, the rate-pressure product at the time to onset of ST depression during overbreathing was similar to that during exercise (152 +/- 24 versus 148 +/- 42; p = NS), whereas in Group II the rate-pressure product at the time to onset of ST depression during recovery was comparable with that under control conditions (104 +/- 30 versus 98 +/- 27; p = NS) and far less than that required to produce ischemia during exercise (104 +/- 30 versus 201 +/- 56; p less than 0.0011). In nine Group III patients, the acute administration of propranolol prevented the early hyperventilation-induced ST segment depression, whereas nifedipine abolished the delayed hyperventilation-induced ST segment depression. These findings suggest that early hyperventilation-induced ST segment depression is due to increased oxygen demand in patients with poor coronary reserve and may be prevented by beta-adrenergic blockers, which are useful for lowering oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of propranolol and verapamil alone and in combination on left ventricular function and volumes in patients with chronic exertional angina: a double-blind, placebo-controlled, randomized, crossover study with radionuclide ventriculography

With the use of equilibrium radionuclide ventriculography the effects on left ventricular (LV) function of 160 mg oral propranolol daily and 360 mg verapamil daily alone and in combination were compared in 18 patients with chronic exertional angina. A randomized, double-blind, placebo-controlled, crossover protocol was used. The reduction in exercise rate-pressure product induced by the combination (118 +/- 28 mm Hg/min) was significantly greater (p less than .05) than that by propranolol (135 +/- 27 mm Hg/min) or verapamil alone (163 +/- 28 mm Hg/min). In patients at rest, neither single nor combined therapy altered global or regional left ventricular ejection fractions (EFs). Verapamil, but not propranolol, increased (p less than .05) cardiac volumes of resting subjects; used in combination, no further increase in LV volume occurred. With placebo, exercise global EF did not decrease from the level at rest and therefore no drug effect could be demonstrated for this parameter of LV function. By an evaluation of normalized regional EF measurements the combination was shown to reduce exercise-induced hypokinesis (placebo 52 +/- 20%, combination 61 +/- 23%; p less than .01). No significant improvement was noted with propranolol or verapamil alone; only the combination prevented a significant increase in end-systolic and end-diastolic volumes during exercise. Thus, propranolol and verapamil, used alone in moderate doses, exert no beneficial effect on exercise LV function as measured by EF and volume changes, and resting function deteriorates slightly with verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)     

Significance of exercise induced ST elevation in patient without a history of previous myocardial infarct

Between 1980 and 1995, we observed twenty-five patients (22 males, 3 females) at the mean age of 50.6 +/- 13 years, without previous myocardial infarction who presented exercise induced ST elevation on a bicycle stress test. METHODS: Significant ST elevation was defined as a > or = 1 mm change present in > or = 1 lead measured 0.08 sec after the J point and in 3 consecutive beats. All patients have undergone coronary angiography in the days following the exercise test. RESULTS: Most of patients (56%) presented a history of typical angina that was either purely exertional (8 pts) or also occurred at rest (6 pts). Others (36%) had non typical angina or no angina (8%); 78% of pts were smokers. Sixteen patients (group I) had ST elevation during exercise (exercise duration: 7.6 +/- 4 min; peak heart rate: 135.5 +/- 29 batt/min; ST = 3.5 +/- 1.5 mm) and nine (group II) during the recovery phase (exercise duration 16.3 +/- 1.6 min; p < 0.05; peak heart rate 168 +/- 22 batt/min; p < 0.05; ST: 5.8 +/- 3 mm; p < 0.05). In group I, 1 patient had no vessel disease, 12 had one vessel disease, 3 had multivessel disease with 6 cases of hypersevere coronary stenose (> 90%). In group II, 4 patients had normal coronary arteries, there was one vessel coronary artery disease in 4 patients and multivessel in one subject, without hypersevere coronary stenosis. Correlation between anatomic location of stenosis and electrocardiographic ST elevation was excellent, particularly in case of single vessel disease (100%). All patients underwent one or more new exercise tests after therapeutic intervention (surgery n = 3; angioplasty n = 7; medical treatment n = 15), only 2 patients had persistent exercise induced ST elevation. During follow-up (5 +/- 3 years), 3 patients died (2 cardiac deaths) and 3 had recurrent angina controlled by new treatment. CONCLUSION: Exercise-induced ST elevation is a rare phenomenon in patients without prior myocardial infarction. When occurring purely during exercise, coronary lesions are frequent and often servere, in the other hand ST elevation of the recovery phase is frequently associate with normal arteries or less severe lesions. In most cases, revascularisation or medical therapy can abolish clinical and electrocardiographic abnormalities.     

Effects of nifedipine on arterial oxygenation at rest and during exercise in patients with stable angina

The effects of nifedipine on arterial oxygenation and hemodynamics were studied at rest and during bicycle exercise in 12 men (mean age 55 years, range 41 to 67) with stable exertional angina. The study was conducted double-blind on 2 days, 1 week apart, using a placebo-controlled crossover design. On each day, measurements at rest were made before and 20 minutes after 20 mg sublingual nifedipine or placebo and were followed by measurements made during exercise. Compared with placebo, nifedipine reduced mean arterial pressure, systemic vascular resistance and pulmonary vascular resistance, and increased heart rate and cardiac output at rest and during exercise. It did not alter mean pulmonary artery or pulmonary artery wedge pressures at rest, but decreased them during exercise. Nifedipine decreased arterial oxygen tension (PaO2) from 96 +/- 10 to 90 +/- 13 mm Hg (p less than 0.05) at rest and from 99 +/- 11 to 92 +/- 12 mm Hg (p less than 0.005) at submaximal exercise (33 +/- 21 W), but did not alter it (100 +/- 12 versus 100 +/- 16 mm Hg, p = NS) at maximal exercise (68 +/- 30 W). The reduction in PaO2 was not due to alveolar hypoventilation, because nifedipine did not alter arterial carbon dioxide tension, or to changes in mixed venous oxygen tension, which nifedipine increased at rest (39 +/- 2 versus 43 +/- 3 mm Hg, p less than 0.001) and during submaximal exercise (31 +/- 4 versus 33 +/- 4 mm Hg, p less than 0.03) and maximal exercise (27 +/- 3 versus 31 +/- 3 mm Hg, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Age- and gender-related changes in exercise left ventricular function in mitral valve prolapse

The correlates of exercise left ventricular (LV) performance were examined in 45 patients with isolated mitral valve prolapse (no associated mitral regurgitation or coronary artery disease). There were 18 men and 27 women, aged 16 to 73 years; 20 patients were 40 years or younger and 25 were older than 40. The response of the LV ejection fraction (EF) to symptom-limited upright exercise was normal (at least a 5% increase) in 27 patients (60%) and abnormal in 18 (40%). There were no significant differences between patients with normal and abnormal EF response in clinical presentation, electrocardiographic findings (at rest or during exercise), medications, rest EF, heart rate (at rest or during exercise) and systemic arterial pressure (at rest and during exercise). A normal EF response was observed more frequently in patients 40 years or younger than in those older than 40 (80 vs 44%, p less than 0.01), and more often in men than in women (78 vs 48%, p less than 0.04). The change in EF from rest to exercise was 18 +/- 9% in men and 5 +/- 10% in women 40 years or younger (p less than 0.01), and 9 +/- 8% in men and 2 +/- 8% in women older than 40 (p less than 0.04). Thus, patients (especially women and those older than 40 years) with isolated mitral valve prolapse may have abnormal LV functional reserve. Genetic differences in the expression of the disease in both sexes and age-related irreversible myocardial changes may explain these observations.