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Biomedical subjects

S E Epstein

Publications and source records attributed to S E Epstein.

At least 127 records · Page 7Linked to original sources
PubMed1989

Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy.

Recent studies indicate that reversible 201Tl perfusion defects, compatible with silent myocardial ischemia, commonly develop during exercise in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy (HCM). To determine whether this represents a dynamic process that may be modified favorably by medical therapy, we studied 29 asymptomatic or minimally symptomatic patients with HCM, aged 12-55 years (mean, 28), with exercise 201Tl emission computed tomography under control conditions and again after 1 week of oral verapamil (mean dosage, 453 mg/day). Treadmill time increased slightly during verapamil (21.0 +/- 3.6 to 21.9 +/- 2.7 minutes, p less than 0.005), but peak heart rate-blood pressure product was unchanged (26.3 +/- 6.0 X 10(3) compared with 25.0 +/- 6.4 X 10(3). Two midventricular short-axis images per study were divided into five regions each, and each of these 10 regions was then analyzed on a 0-2 scale by three observers blinded with regard to the patients' therapy. Average regional scores of 1.5 or less were considered to represent perfusion defects, and a change in regional score of 0.5 or more was considered to constitute a significant change. During control studies, 15 patients (52%) developed perfusion defects with exercise (average, 3.7 regions per patient). In 14 of these patients, all perfusion defects completely reversed after 3 hours of rest; one patient had fixed defects. After administration of verapamil, exercise perfusion scores improved in 10 of the 14 patients (71%) with reversible defects; there was overall improvement in 34 of 50 (68%) regions with initially reversible perfusion defects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Electrophysiologic abnormalities in patients with hypertrophic cardiomyopathy. A consecutive analysis in 155 patients.

Electrophysiologic studies (EPS) were performed in 155 patients with hypertrophic cardiomyopathy (HCM). Indications for EPS were cardiac arrest in 22 patients, syncope in 55 patients, presyncope in 37 patients, asymptomatic ventricular tachycardia (VT) in 24 patients, palpitations in 10 patients, and a strong family history of sudden cardiac death in seven patients. Thirty-five (23%) patients had significant resting left ventricular outflow tract obstruction. Electrophysiologic abnormalities were present in 126 (81%) patients. A high prevalence of abnormal sinus-node function (66%) and His-Purkinje (HV) conduction (30%) was noted. The most commonly induced supraventricular arrhythmias were atrial reentrant tachycardia and atrial fibrillation (10% and 11% of patients, respectively). Accessory atrioventricular pathways were present in seven (5%) patients. Programmed ventricular stimulation (PVS) induced nonsustained ventricular tachycardia in 22 (14%) patients and sustained ventricular arrhythmia in 66 (43%) patients. Sustained ventricular arrhythmia was polymorphic VT in 48 (73%) patients, monomorphic VT in 16 (24%) patients, and ventricular fibrillation in two (3%) patients. Induction was with two premature stimuli in 19 (29%) patients and three premature stimuli in 47 (71%) patients. Of 17 cardiac arrest survivors with sustained ventricular arrhythmia, 16 (94%) patients required three premature stimuli for arrhythmia induction. Sustained ventricular arrhythmia was induced at a right ventricular site in 51 (77%) patients and at a left ventricular site in 15 (23%) patients. Univariate analysis showed a significant (p less than 0.05) association between inducibility of sustained ventricular arrhythmia and VT on Holter in patients with a history of cardiac arrest or syncope but not in patients with presyncope or asymptomatic patients. Multivariate logistic regression analysis revealed that the following were significantly associated with inducibility of sustained ventricular arrhythmia: clinical presentation (cardiac arrest more than syncope more than presyncope more than asymptomatic patients, p = 0.0002; chronic or inducible atrial fibrillation, p = 0.002; and male gender, p = 0.04). In contrast, there was no clinical correlate of induced nonsustained VT.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Contrasting effects of verapamil and nifedipine on pH of ischemic myocardium in the dog.

It remains unknown whether the actions of verapamil to depress and nifedipine to enhance contractile function of ischemic myocardium influence the degree of myocardial ischemic injury. Thus, we measured intramyocardial pH using fiberoptic pH probes in 43 anesthetized open-chest dogs pretreated for 30 min with verapamil, or nifedipine in doses that decreased aortic pressure 10 to 15 mm Hg before ligation of the left anterior descending coronary artery for 15 min. Drugs were continued during the 15-min ischemic period until the animals were euthanized without reperfusion: verapamil, 10-20 micrograms/kg/min and nifedipine, 2 to 4 micrograms/kg/min i.v. Verapamil-treated dogs showed higher pH of ischemic subendocardium after 15 min ischemia (6.75 +/- 0.07) than did the nifedipine (6.48 +/- 0.04) or placebo (6.43 +/- 0.05) groups, even if the animals were paced (6.71 +/- 0.11) to prevent the negative chronotropic effect of verapamil (P less than 0.01). Neither verapamil nor nifedipine changed collateral myocardial blood flow from 0.10 +/- 0.02 in the subendocardium and 0.17 +/- 0.03 ml/min/g in the subepicardium. Left ventricular function estimated by left ventricular dp/dt was depressed 15% by verapamil and enhanced 26% by nifedipine. Thus, verapamil, but not nifedipine, relieves acidosis of ischemic myocardium after acute coronary occlusion in doses that sustain a 10 to 15 mm Hg decrease in aortic pressure. Nifedipine, in doses that produced the same 10 to 15 mm Hg decrease in mean aortic pressure, did not increase intramyocardial pH, as it enhanced contractile function, estimated by left ventricular dp/dt.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy.

When angina occurs in patients with hypertension, it is usually attributed to coronary artery disease or left ventricular hypertrophy. To determine the contribution of coronary microvascular abnormalities to angina in patients with hypertension, we evaluated hypertensive patients without coronary artery disease or left ventricular hypertrophy by measuring the coronary responses to rapid atrial pacing before and after administration of ergonovine. We compared 12 hypertensive patients who had pacing-induced angina with 13 normotensive subjects without such angina. The two groups had similar coronary flow (in the great cardiac vein) at rest; however, pacing increased coronary flow less in hypertensive patients with angina than in normotensive subjects (48 vs. 83 percent; P = 0.05). In the hypertensive patients with angina, pacing after ergonovine increased coronary flow by only 32 percent (as compared with 48 percent before ergonovine; P less than 0.05) and decreased coronary resistance by 15 percent (as compared with 28 percent before ergonovine; P less than 0.05), indicating the presence of ergonovine-induced vasoconstriction. In normotensive subjects, in contrast, cardiac pacing after ergonovine increased coronary flow by 112 percent (P less than 0.001), and its effect on coronary resistance was not different from that of pacing before ergonovine. The hypertensive patients with angina had a significant increase in myocardial oxygen extraction during pacing after ergonovine and less of an increase in myocardial lactate consumption - a response consistent with the presence of myocardial ischemia. Thus, angina in hypertensive patients without epicardial coronary disease may be caused by myocardial ischemia, which appears to be due to an abnormally elevated resistance of the coronary microvasculature.

Angina Pectoris↗
PubMed1988

Long-term serial changes in left ventricular function and reversal of ventricular dilatation after valve replacement for chronic aortic regurgitation.

In most patients with aortic regurgitation, valve replacement results in reduction in left ventricular dilatation and an increase in ejection fraction. To determine the relation between serial changes in ventricular dilatation and changes in ejection fraction, we studied 61 patients with chronic severe aortic regurgitation by echocardiography and radionuclide angiography before, 6-8 months after, and 3-7 years after aortic valve replacement. Between preoperative and early postoperative studies, left ventricular end-diastolic dimension decreased (from 75 +/- 6 to 56 +/- 9 mm, p less than 0.001), peak systolic wall stress decreased (from 247 +/- 50 to 163 +/- 42 dynes x 10(3)/cm2), and ejection fraction increased (from 43 +/- 9% to 51 +/- 16%, p less than 0.001). Between early and late postoperative studies, diastolic dimension and peak systolic wall stress did not change, but ejection fraction increased further (to 56 +/- 19%, p less than 0.001). The increase in ejection fraction correlated with magnitude of reduction in diastolic dimension between preoperative and early postoperative studies (r = 0.63), between early and late postoperative studies (r = 0.54), and between preoperative and late postoperative studies (r = 0.69). Late increases in ejection fraction usually represented the continuation of an initial increase occurring early after operation. Thus, short-term and long-term improvement in left ventricular systolic function after operation is related significantly to the early reduction in left ventricular dilatation arising from correction of left ventricular volume overload. Moreover, late improvement in ejection fraction occurs commonly in patients with an early increase in ejection fraction after valve replacement but is unlikely to occur in patients with no change in ejection fraction during the first 6 months after operation.

Adult↗
PubMed1987

Impaired forearm vasodilator reserve in patients with microvascular angina. Evidence of a generalized disorder of vascular function?

In previous work, we described a group of patients with angina-like chest pain and normal coronary arteries. These patients had impaired coronary vasodilator responses to the stress of rapid atrial pacing and to the administration of dipyridamole, a potent vasodilator of coronary arterioles. This abnormality appears to be localized to the prearteriolar microvascular bed. To determine whether these patients have a more generalized abnormality of vasodilator reserve, we used mercury-in-Silastic strain-gauge plethysmography to compare their hyperemic responses to forearm ischemia with those of normal controls. After 10 minutes of ischemia, peak forearm flow was 39.9 +/- 5.0 ml per minute per deciliter in the controls [corrected] and 31.7 +/- 10.5 in the patients [corrected] (21 percent reduction; 95 percent confidence interval, 4 percent to 37 percent). Flow responses were also significantly reduced after three and five minutes of ischemia. Correspondingly, the vascular resistance after ischemia was also consistently higher in the patients with microvascular angina. The degree of vasodilator impairment in the peripheral circulation correlated well with the degree of vasodilator impairment in the coronary circulation (r = 0.74; P less than 0.004). Thus, patients with microvascular angina appear to have an impairment of vasodilator reserve that affects not only their coronary circulation but also their peripheral arterial bed.

Adult↗
PubMed1987

Prognostic implications of symptomatic versus asymptomatic (silent) myocardial ischemia induced by exercise in mildly symptomatic and in asymptomatic patients with angiographically documented coronary artery disease.

Patients with coronary artery disease (CAD) may undergo periods of reversible myocardial ischemia without experiencing angina. To study the prognostic implications of "silent" myocardial ischemia induced by exercise, exercise electrocardiography and radionuclide angiography were performed in 131 consecutive patients with CAD, preserved left ventricular (LV) function at rest and mild or no symptoms during medical therapy. All patients who died during medical therapy were in the subgroup of patients with 3-vessel CAD in whom exercise-induced ischemia developed, which was characterized by both a decrease in LV ejection fraction and ST-segment depression. Patients in whom angina pectoris developed during exercise (54% of all patients) had a greater prevalence of this combined ischemic response to exercise than patients without angina (61% vs 27%, p less than 0.001) and also a greater prevalence of left main or 3-vessel CAD (59% vs 25%, p less than 0.001). However, when inducible ischemia was demonstrated, risk stratification and prognosis were the same whether the ischemic episode was symptomatic or silent. Among patients having both a reduction in ejection fraction and a positive ST-segment response, the likelihood of significant left main narrowing (13% vs 26%), 3-vessel CAD (56% vs 51%) and death during subsequent medical therapy (16% vs 9%) was similar in patients with silent compared to those with symptomatic ischemia. These data indicate that patients in whom angina develops during exercise have a greater prevalence of high-risk coronary anatomy and of inducible ischemia than patients without angina. However, once inducible ischemia is documented, the symptomatic response to exercise appears irrelevant for prognostic or risk stratification considerations.

Aged↗
PubMed1987

Occurrence and significance of progressive left ventricular wall thinning and relative cavity dilatation in hypertrophic cardiomyopathy.

This investigation was undertaken to assess the prevalence of systolic dysfunction, left ventricular (LV) wall thinning and cavity enlargement in a large population of patients with hypertrophic cardiomyopathy (HC), and to determine the role of these conditions in the natural history of this disease. Of 217 consecutively studied patients with HC, most of whom were severely symptomatic, 197 (91%) had an LV ejection fraction of 50% or more and 20 (9%) had an ejection fraction of less than 50% as assessed with radionuclide angiography. Changes in LV wall thickness and cavity dimension were evaluated using serial M-mode and 2-dimensional echocardiography over an average follow-up of 3.6 years in 67 of the 217 patients (54 with ejection fraction of greater than or equal to 50% and 13 with ejection fraction less than 50%). A substantial decrease (at least 5 mm) in LV wall thickness was seen in 8 of the 13 patients (62%) with an ejection fraction greater than or equal to 50%, but in only 2 of the 54 patients (4%) with an ejection fraction greater than or equal to 50% (p less than 0.001). LV cavity dimension increased significantly over the period of follow-up in the 13 patients with depressed ejection fraction (from 44 +/- 5 to 49 +/- 7 mm, p less than 0.005); however, absolute cavity size remained normal (less than or equal to 52 mm or less) in 10 of these 13 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Low density lipoprotein modulation of porcine coronary artery contractile response to histamine.

Right coronary artery ring segments from miniature swine contracted to histamine with a force and sensitivity comparable to that reported for human right coronary artery ring segments. When the ring segments were suspended in preparations of human low density lipoprotein (LDL) the contractility was reduced. With denuded rings the contractility was significantly lower in the LDL at 1.1 X 10(-4) M histamine. With intact rings significantly less tension was generated in the LDL at concentrations greater than 6 X 10(-5) M histamine. Thus LDL attenuates the contractile response of the porcine right coronary artery to histamine.

Animals↗
PubMed1987

Determinants of ventricular arrhythmias in mildly symptomatic patients with coronary artery disease and influence of inducible left ventricular dysfunction on arrhythmia frequency.

To determine the relation among ventricular arrhythmias, prognostic factors and reversible ischemia in coronary artery disease, 131 drug-free, minimally symptomatic patients were studied by radionuclide angiography and 24 hour Holter electrocardiographic monitoring. High grade ventricular arrhythmias (couplets, salvos of premature ventricular complexes and R on T phenomenon) were observed in 33 patients (25%) and were related to lower rest and exercise ejection fraction, greater number of stenotic coronary arteries and higher prevalence of regional wall motion abnormalities at rest (all p less than or equal to 0.1). Among patients with subnormal rest ejection fraction, high grade arrhythmias occurred with greater prevalence in those with reversible left ventricular dysfunction (reduction in ejection fraction) during exercise compared with those with a normal ejection fraction response (59 versus 23%, p less than 0.05), a relation observed principally in patients with multivessel disease. These data indicate that in minimally symptomatic patients with coronary artery disease, arrhythmias are related to both extent of disease and severity of regional and global ventricular dysfunction and are most prevalent in patients with ventricular dysfunction and evidence of inducible ischemia, factors indicating poor long-term prognosis during medical therapy.

Adult↗
PubMed1987

Three year anatomic, functional and clinical follow-up after successful percutaneous transluminal coronary angioplasty.

Because the long-term anatomic effects of percutaneous transluminal coronary angioplasty are unknown, follow-up evaluations including coronary angiography, treadmill exercise testing and rest and bicycle exercise radionuclide angiography were performed in 46 patients 6.3 +/- 2.0 and 37.6 +/- 3.6 (mean +/- SD) months after they had undergone successful single lesion angioplasty. The severity of the coronary stenosis decreased significantly at each evaluation; the mean diameter stenosis was 66 +/- 13% before angioplasty, 30 +/- 13% immediately after and 26 +/- 16% and 19 +/- 13% at 6 months and 3 years, respectively. Exercise time increased from 9.8 +/- 4.4 minutes before angioplasty to 18.3 +/- 4.5 minutes immediately after the procedure and remained at that level at 6 months (20.3 +/- 4.6 minutes) and 3 years (18.2 +/- 4.5 minutes). Left ventricular ejection fraction during exercise decreased 4 +/- 6% compared with rest before angioplasty, but increased 7 +/- 7% immediately after angioplasty and this increase was maintained at 6 months (+/- 6 +/- 7%) and 3 years (+/- 4 +/- 6%). Before angioplasty, 1 patient was in Canadian Heart Association functional class 0, 15 were in class II, 24 in class III and 6 in class IV. Three years later, 25 were in class 0, 10 in class I, 7 in class II and 4 in class III. These results indicate that the short-term anatomic and functional success of coronary angioplasty is maintained for at least 3 years.

Adult↗