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Fifty-eight of 220 consecutive patients had exercise-induced ST depression in some or all precordial leads 3 to 12 months after a first inferior myocardial infarction. All 58 patients underwent thallium-201 exercise testing, 2-dimensional echocardiography and coronary angiography. ST depression was confined to leads [V.sub.1-4] in 22 patients (group A); thallium-201 exercise testing showed reversible anterior perfusion defects and left anterior descending coronary artery disease in 11 of the 22 patients (5O%). None of the other 11 with negative thallium-201 exercise test results had significant left anterior descending narrowing, and the anterior ST depression could be explained by asynergy of the posterior wall found on 2-dimensional echocardiograpyhy in 10. ST depression appeared in leads [V.sub.5-6] in 22 patients (group B); reversible anterior perfusion defects and left anterior descending disease was demonstrated in 18 patients (82%). In the other 4 patients posterior wall asynergy was demonstrated. ST depression was seen from leads [V.sub.1-6] in 14 patients (group C); reversible anterior perfusion defects were seen in 6 patients (430%), 5 of whom had significant left anterior demanding disease. Among the other 8 patients without reversible versible anterior perfusion defects, posterior wall asynergy was found in 6. Thus, (1) exercise-induced ST depression in leads [V.sub.5-6] had a high positive predictive value (82%) for left anterior descending disease, higher than ST depression in [V.sub.1-4] or in [V.sub.1-6]; (2) exercise-induced anterior ST depression in patients without a reversible anterior perfusion defect on thallium-201 scintigraphy is usually due to a 'reciprocal' mechanism, i.e., posterior wall asynergy (mainly hypokinesia, which was demonstrated on 2-dimensional echocardiogaphy).

Diastolic function is routinely assessed using Doppler-derived left ventricular (LV) filling patterns. Ratios between peak flow velocities during early filling and atrial contraction (E/A) of 2 was found in 5 patients (13%) and in only 1 control subject; 19 patients (50%) had an apparently normal E/A ratio. No correlation was found between LV filling pattern and ejection fraction or presence of diabetes or arterial hypertension. LV end-diastolic pressures were low to normal in patients with an E/A ratio 15 mm Hg in those with normal or abnormally increased (>2) E/A ratios. Thus, an apparently normal E/A ratio in patients after myocardial infarction may identify those with more severe LV diastolic dysfunction and increased LV filling pressure. (Am J Cardiol 1992;70:711-714)

To determine the relation between myocardial ischemic indexes on exercise testing and on ambulatory Holter recording, 60 patients with stable coronary artery disease who exhibited an ischemic response to both testing procedures were studied. All patients performed a Bruce protocol exercise test and underwent 24-hour Holter recording within 2 weeks without antianginal medications. Mean exercise duration was 7.4 +/- 2.8 minutes, mean heart rate at 1 -mm ST depression was 118 +/- 20 beats/min and mean maximal ST depression during exercise was 2.2 +/- 1 mm. During Hofter recording the average number of ischemic episodes was 4.7 +/- 2.6 per patient, mean duration of dally ischemia was 62 +/- S4 minutes, mean maximal ST depression was 3.2 +/- 1.3 mm and average heart rate at 1mm ST depression was 93 +/- 17 beats/min. Overall, the correlations between ischemic indexes on both testing procedures were very weak (mean r.sup.2 = O.Or4). The only exercise variable that had a significant correlation (p Thus, ischemic indexes on exercise testing cannot accurately predict ischemic indexes on ambulatory Holter recording in patients with stable coronary artery disease who exhibit ischemic changes on both tests. These findings indicate that a great portion of the variability of Holter ischemic indexes is dependent on factors other than those represented by exercise testing indexes, and that Holter recording in the ambulatory setting might provide clinically relevant information in addition to that obtained by exercise testing in selected subsets of patients. (Am J Cardiol 1991;68:176-180), Coronary artery disease is a condition in which the arteries supplying blood to the heart become clogged, usually with fatty atherosclerotic deposits. The resulting diminution of cardiac blood supply (myocardial ischemia) can cause pain and damage to the heart. During exercise, when the workload on the heart is increased, the ischemia is frequently made worse. The relationship between the prevalence of episodes of ischemia during standardized hospital exercise testing and during everyday activities is not known; it is assumed that the former predicts the latter with a reasonable degree of accuracy, but well controlled studies on which this assumption can be based have not been done. To further investigate the relationship between ischemia during exercise testing and during normal daily activities, a study was carried out involving 60 patients with documented, stable coronary artery disease, all of whom exhibited myocardial ischemia both during the course of everyday exercise and during formal exercise testing. Exercise testing lasted an average of 7.4 minutes, during which all patients exhibited ischemia (as indicated by characteristic changes in the electrocardiographic record). During 24-hour ambulatory monitoring of cardiovascular parameters, patients experienced ischemia for an average of 62 minutes (4.7 episodes per patient). Overall, the correlations between indices of ischemia in exercise-induced and spontaneous situations were very weak. Hence, ischemic indices on exercise testing do not accurately predict ischemic indices during everyday activities, and 24-hour ambulatory monitoring can provide useful clinical data which exercise testing does not yield. (Consumer Summary produced by Reliance Medical Information, Inc.)

The antiischemic properties of nisoldipine, a dihydropyridine calcium antagonist, were assessed in a multicenter, double-blind, placebo-controlled trial by repeated exercise testing and 72-hour ambulatory electrocardiographic monitoring in 82 patients with coronary artery disease. Patients with positive treadmill stress test results and [greater than or equal to 2 ischemic episodes per 24 hours were included in this study. Administration of all chronic antiischemic medications except [Beta] blockers were discontinued. During the first week all patients received placebo twice daily. During the second and third weeks, 41 patients received nisoldipine 10 mg and 41 patients received placebo twice daily. in the placebo group there were no changes in exercise parameters or in ambulatory electrocardiographic parameters. In the nisoldipine group, exercise duration increased from 403 to 448 seconds (p = 0.0035), time to 1 mm of ST depression increased from 224 to 298 seconds (p = 0.002), time to pain increased from 241 to 321 seconds (p = 0.01), and maximal ST depression was reduced from 2.6 to 2.3 mm (p = 0.002). Among the ambulatory electrocardiographic parameters in the nisoldipine group, only the number of episodes was reduced, from 14.4 to 11.6 (p = 0.0013) per patient. There was no significant reduction in total ischemic time (132 vs 120 minutes per patient). No significant side effects were observed. This is the largest clinical trial to date on the effects of nisoldipine on myocardial ischemia. The results indicate that nisoldipine was effective in improving all exercise parameters and only partially effective in suppressing ischemia during daily activity. (Am J Cardiol 1991;67:559-564), Coronary artery disease (CAD) is a condition in which the arteries supplying blood to the heart become occluded, most frequently with fatty atherosclerotic (fat-containing hardened material) deposits that build-up on the arterial walls. The resulting decrease in the cardiac blood supply (myocardial ischemia) can cause chest pain (angina pectoris) and damage to the heart muscle. Drug treatment of this condition frequently takes the form of coronary vasodilating drugs, which cause relaxation of the coronary arteries, and calcium channel blocking drugs, which induce vasodilation by blocking the entry of calcium into muscle fibers. To assess the anti-ischemic effects of nisoldipine, a dihydropyridine calcium channel blocker, a multicenter study was carried out with 82 patients with known CAD. Patients were subjected to 72-hour ambulatory electrocardiographic monitoring (to record the electrical activity of the heart) with repeated exercise testing, following discontinuation of all chronic anti-ischemic medications except beta blockers. The study was conducted over a three-week period; patients received an inactive placebo the first week, and were randomly assigned to receive either nisoldipine or placebo during the second and third weeks. There were no changes in exercise or electrocardiographic parameters in placebo-treated patients, but nisoldipine caused increases in the length exercise periods, the time to onset of pain, and time to onset of electrocardiographic abnormalities. Although the number of ischemic episodes was reduced in nisoldipine-treated patients, there was no significant difference in total ischemic time between the two groups. No serious side effects were observed with the doses of nisoldipine used in the study. (Consumer Summary produced by Reliance Medical Information, Inc.)

This study assesses the variations in myocardial ischemic threshold (heart rate at the onset of ischdemia) during dally activities in patients with ischemic episodes on Holter monitering. Eighty patients with known coronary artery disease, positive treadmill stress test results and >2 ischemic episodes during a 24-hour period of Holter monitoring were studied. The lowest and the highest ischemic thresholds were determined for each patient. The mean lowest ischemic threshold was 85 beats/min, and the mean highest ischemic threshold was 109 beats/min. The highest ischemic threshold was identical to ischemic threshold values noted during exercise. Of the 89S ischemic episodes, 6S4 (74%) were preceded by a moderate >10%) increase in heart rate. The variability of ischemic threshold difference in percentage between the highest and lowest ischemic thresholds) increased with the number of ischemic episodes (range 2 to 60%). However, in different patients with a similar number of ischemic episodes, different variability was observed. These differences in ischemic thresholds are probably indirect indicators of the vasomoter activity of the coronary arteries in different patients. (Am J Cardiol 1990;66-1403-1406), Myocardial ischemia is a pathological diminution of the blood flow to the heart. This occurs frequently in cases of coronary artery disease, in which the blood vessels supplying the heart are narrowed (stenotic) to the point that blood flow is occluded. The condition may not produce symptoms in sedentary individuals, but is usually revealed when cardiac function is measured during exercise. As heart rate increases, the metabolic demands of the heart rise, and the narrowed arteries are unable to accommodate the volume of blood necessary to supply the organ. Within a given patient, the point at which ischemia develops during exercise testing (myocardial ischemic threshold) is constant. It has been reported that, in patients undergoing ambulatory monitoring of cardiac function, ischemia can develop at variable heart rates which are significantly lower than the threshold determined by exercise testing. To investigate this more fully, 80 patients with known coronary artery disease were monitored for the incidence of myocardial ischemia during their daily activities. The average lowest ischemic threshold was 85 beats per minute, and the average highest ischemic threshold was 109 beats per minute, which was identical to the threshold determined during exercise testing. Seventy-four percent of the ischemic episodes (654 out of 895) were preceded by a moderate (greater than 10 percent) increase in heart rate. As the number of occurrences of ischemia increased, so did the variability in the threshold (ranging from 2 to 60 percent), and the extent to which this occurred varied from patient to patient. The reason for this difference in ischemic threshold may be the differential vasoconstriction (constriction of the coronary arteries caused by nerves and hormones) in different patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Disopyramide is a drug given to patients with abnormal heart rhythms. The physiological effect of disopyramide during pregnancy has been questioned. To see if disopyramide can cause contractions of the uterus significant enough to induce labor, 10 women were given disopyramide or a placebo, 48 hours before planned labor induction for other medical reasons. In the group receiving disopyramide, 10 patients had contractions and eight patients delivered within 48 hours. There were no contractions noted in any of the ten patients receiving the placebo and no deliveries. The time it took for the onset of regular uterine contractions was 4.15 hours, compared with 56.13 hours in the nontreated group. The levels of disopyramide during labor contractions were significantly lower than the levels required to prevent abnormal heart rhythms. There were no significant side effects of disopyramide in the mother or fetus. It is unlikely that disopyramide would be a candidate for a labor-inducing drug, since it did not initiate labor in two women. In addition, the duration of labor was prolonged when compared with other agents. Disopyramide should not be used to prevent abnormal heart rhythms in pregnant cardiac patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Atrial septum aneurysm (ASA), usually involving the region of the fossa ovalis, has rarely been de. scribed in children. In this study, the incidence and natural course of this anomaly were prospectively evaluated in 3,500 children referred for echocardioqraphic examination. ASA was found in 35 patients, 19 female and 16 male (1.0%). Patients were 6 years of age or younger at the time of diagnosis and 18 were neonates. None of the 750 children with normal echocardiograms had ASA. The most common associated lession was atrial septal defect (ASD), which occurred in 24 of the 35 patients (69%). Other associated cardiac lessions were ventricular septal defect in 10, pulmonary stenosis in 5, patent ductus arteriosus in 4 and coarctation or interruption of the aorta with subaortic membrane in 2. No clinical complications were associated with ASA. Six patients with complex heart disease died. When associated with ASD, the direction of the ASA motion and that of the shunt found by Doppler echocardiography were similar. Fourteen patients with ASD were followed for 0.5 to 4 years. In 8 the ASD closed and in 6 the ASA disappeared. in 6 patients the ASD and ASA persisted until the end of the follow-up (p [is less than] 0.01). Thus, the incidence of ASA in children in this series was higher than previously presumed and usually was associated with other cardiac anomalies, mainly ASD. In children, ASA tends to disappear with age and may have a role in spontaneous closure of associated ASD. (Am J Cardiol 1989;64.IM-1001), The septum is the thick wall of tissue that separates the right side of the heart from the left. The atrial septum is located between the atria, the two chambers that receive blood from the body (right atrium) or lungs (left atrium) before pumping it to the ventricles. Like almost all components of the circulatory system, the atrial septum can develop an aneurysm (atrial septal aneurysm, ASA), a bulge in the wall that protrudes into either or both atria. This is usually found in association with other cardiac abnormalities. Atrial septal aneurysm is uncommon in adults and has been observed very infrequently among children, but may be underdiagnosed in children. Over a period of more than four years, the incidence, characteristics, and consequences of ASA were observed in a group of 3,500 children between the ages of one day and 15 years. Using criteria that took into account echocardiographic (ultrasound) and anatomic evidence, researchers defined two types of ASA. Patients with Type 1 ASA had the aneurysm only in the region of the fossa ovalis, a small indentation in the septum where an actual opening is located during fetal life, while Type 2 ASA patients had atrial protrusion along the entire length of the septum. Atrial septal aneurysm was found in 35 children (1 percent), of whom 18 were newborn. All these patients had been referred because a heart murmur had been detected and all had congenital heart defects, with atrial septal defect (ASD) the most common. When some patients were followed-up, ASA disappeared in 45 percent of 20 patients, and among patients with both ASA and ASD, the ASA disappeared in those whose atrial septal defect spontaneously closed, but it remained when ASD remained. These results indicate that the incidence of ASA is higher than previously suspected and that the condition often disappears with age. Since ASA was associated with the disappearance of ASD, it may play a role in reduction of that defect. (Consumer Summary produced by Reliance Medical Information, Inc.)