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Biomedical subjects

S O Gottlieb

Publications and source records attributed to S O Gottlieb.

At least 37 records · Page 2Linked to original sources
PubMed1991

Medical therapy of unstable angina pectoris.

The pathophysiologic mechanisms responsible for the clinical syndrome known as unstable angina pectoris are complex but provide a framework for a rational medical approach to this ischemic condition. The combined use of nitrates, beta-blockers, calcium antagonists, antiplatelet agents, and anticoagulants has been shown to reduce recurrent ischemia, and the latter therapies have reduced the incidence of progression to myocardial infarction and death. A rational risk stratification scheme, which utilizes the presenting symptoms, electrocardiographic, and anatomic information to identify patients for whom additional revascularization procedures are warranted, is presented.

Adrenergic beta-Antagonists↗
PubMed1991

Asymptomatic or silent myocardial ischemia in angina pectoris: pathophysiology and clinical implications.

Patients with angina pectoris often have asymptomatic myocardial ischemia, which can be detected by exercise testing, ambulatory (Holter) monitoring, and other diagnostic methods. Studies suggest that the presence of frequent and prolonged episodes of ischemia are associated with an adverse prognosis. Standard antiangina strategies have been found to be effective in reducing exercise and spontaneous episodes of ischemia. However, whether the targeted suppression of all ischemic activity should be a therapeutic goal remains unresolved and is the focus of current research efforts.

Angina Pectoris↗
PubMed1991

Preventive maintenance of the aging heart.

Coronary heart disease (CHD) is the major cause of mortality in the elderly. Important risk factors include hypercholesterolemia, systolic and diastolic hypertension, cigarette smoking, hyperglycemia, and obesity. Elderly patients with existing CHD should be treated aggressively to control these risk factors, along with other medical therapies to treat myocardial ischemia. For elderly patients without recognized CHD, however, a more conservative approach is recommended and includes behavioral interventions when appropriate and pharmacologic therapy for higher risk patients with persistent, uncontrolled risk factors.

Aged↗
PubMed1990

The effects of antihypertensive therapy on left ventricular mass in elderly patients.

Left ventricular mass sometimes decreases during treatment of hypertension, but this response is inconsistent and its effects on left ventricular function are unknown. In a six-month randomized trial, we studied the ability of verapamil and atenolol to reduce left ventricular mass in 42 elderly patients with hypertension and the effects of this reduction in mass on cardiac function. The mean blood pressure (+/- SE) decreased in both the group that received verapamil (from 171.4 +/- 3.2/93.0 +/- 2.5 mm Hg to 142.9 +/- 2.8/79.0 +/- 2.0 mm Hg) and the group that received atenolol (from 179.6 +/- 4.6/98.5 +/- 2.4 mm Hg to 148.1 +/- 3.3/83.4 +/- 1.2 mm Hg), but the atenolol-treated patients more frequently required the addition of chlorthalidone to achieve blood-pressure reduction (P less than 0.01). Verapamil resulted in a reduction in the left-ventricular-mass index from 104 +/- 5 g per square meter of body-surface area to 85 +/- 5 g per square meter (P less than 0.01). Atenolol did not produce a reduction in the left-ventricular-mass index (109 +/- 9 g per square meter before treatment vs. 112 +/- 10 g per square meter after treatment). Two weeks after the withdrawal of antihypertensive therapy, blood pressure returned to pretreatment values. Nevertheless, in patients whose left ventricular mass had decreased, two measures of diastolic filling, the peak diastolic filling rate to the peak ejection rate, were significantly higher than before treatment (2.42 +/- 0.2 vs. 3.31 +/- 0.4 [P less than 0.05] and 0.61 +/- 0.03 to 0.85 +/- 0.05 [P less than 0.05], respectively). Diastolic filling was unchanged in the group that had no reduction in left ventricular mass. Cardiac output and the ejection fraction at rest and during mild exercise were unchanged in both groups as compared with baseline values. We conclude that left ventricular mass can be reduced in elderly patients with hypertension and mild ventricular hypertrophy who receive antihypertensive therapy. Reduction occurs more frequently with verapamil than with atenolol therapy, increases diastolic filling, and does not impair systolic function.

Atenolol↗
PubMed1990

Frequency and importance of silent myocardial ischemia identified with ambulatory electrocardiographic monitoring in the early in-hospital period after acute myocardial infarction.

The incidence and clinical significance of silent myocardial ischemia occurring in the early period after acute myocardial infarction (AMI) was studied in 59 patients who had an uncomplicated early course after admission for AMI. Calibrated 2-lead ambulatory electrocardiographic monitoring performed for 39 +/- 2 hours starting 4 +/- 1 days after AMI identified silent myocardial ischemia, defined as greater than or equal to 1 mm ST-segment change lasting greater than or equal to 2 minutes, in 27 patients. These patients had 5 +/- 1 episodes lasting a median of 11 minutes/episode (range 2 to 36 minutes/episode). Patients with and without silent ischemia had comparable baseline demographics, were receiving similar anti-ischemic medications and had similar severity of coronary disease by angiography. No reinfarctions occurred during the in-hospital period. Fourteen of 27 patients (52%) with silent ischemia had greater than or equal to 1 in-hospital clinical ischemic event (pulmonary edema, n = 5, cardiac death, n = 1, and postinfarction angina, n = 11). In contrast, only 7 of 32 patients without silent ischemia (22%) had greater than or equal to 1 in-hospital event (pulmonary edema, n = 1, cardiac death, n = 1, and postinfarction angina, n = 6). The frequency of ischemic events was significantly greater in patients with silent ischemia compared to those without silent ischemia, p less than 0.02. Silent ischemia occurs frequently very early after AMI and identifies a group of patients who are at increased risk for adverse in-hospital clinical outcomes.

Coronary Disease↗
PubMed1990

Coronary artery aneurysm formation following percutaneous transluminal coronary angioplasty: treatment of associated restenosis with repeat percutaneous transluminal coronary angioplasty.

Restenosis following coronary angioplasty can usually be treated effectively and safely by repeated angioplasty. However, the presence of a complex lesion morphology may bias the clinician away from angioplasty toward either recommending bypass surgery or continuing medical therapy alone in spite of recurrence of the symptoms which were sufficient indication for the initial angioplasty. One type of complex morphology at the site of the restenosis is due to the presence of a focal, eccentric aneurysmal dilatation similar in appearance to a saccular aneurysm. In two previously reported cases in the literature both were referred to bypass surgery. We report eight additional cases including the use of repeat successful angioplasty in six of the cases in spite of the potential problems posed by the complexity of the restenosed lesion. In addition, this case review suggests that this type of complex lesion morphology with restenosis may be more common when the initial angioplasty was associated with deep arterial injury, as in patients whose initial angioplasty was done in an infarct-related vessel or was associated with evidence of a large dissection.

Adult↗
PubMed1989

Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease.

Patients with atherosclerotic cardiovascular disease may be adversely affected by the presence of carboxyhemoglobin, even at low concentrations. We investigated the effects of carbon monoxide exposure on myocardial ischemia during exercise in 63 men with documented coronary artery disease. On each test day, subjects performed two symptom-limited incremental exercise tests on a treadmill; the tests were separated by a recovery period and 50 to 70 minutes of exposure to either room air or air containing one of two concentrations of carbon monoxide (117 +/- 4.4 ppm or 253 +/- 6.1 ppm). The order of exposure was assigned randomly. On each occasion, neither the subjects nor the study personnel knew whether the subjects had been exposed to room air or to one of the concentrations of carbon monoxide. Exposure to room air resulted in a mean carboxyhemoglobin level of 0.6 percent, exposure to the lower level of carbon monoxide resulted in a carboxyhemoglobin level of 2.0 percent, and exposure to the higher level of carbon monoxide resulted in a level of 3.9 percent. An effect of carbon monoxide on myocardial ischemia was demonstrated objectively by electrocardiographic changes during exercise. We observed a decrease of 5.1 percent (90 percent confidence interval, 1.5 to 8.7 percent; P = 0.02) and a decrease of 12.1 percent (90 percent confidence interval, 9.0 to 15.3 percent; P less than or equal to 0.0001) in the length of time to a threshold ischemic ST-segment change (ST end point) after carbon monoxide exposures that produced carboxyhemoglobin levels of 2.0 percent and 3.9 percent, respectively. The length of time to the onset of angina decreased by 4.2 percent (90 percent confidence interval, 0.7 to 7.9 percent; P = 0.054) at the 2.0 percent carboxyhemoglobin level and by 7.1 percent (90 percent confidence interval, 3.1 to 10.9 percent; P = 0.004) at the 3.9 percent carboxyhemoglobin level. Significant dose-response relations were found in both the change in the length of time to the ST end point (P less than or equal to 0.0001) and the change in the length of time to the onset of angina (P = 0.02). We conclude that low levels of carboxyhemoglobin exacerbate myocardial ischemia during graded exercise in subjects with coronary artery disease.

Adult↗
PubMed1989

Frequency and significance of early postoperative silent myocardial ischemia in patients having peripheral vascular surgery.

Coronary disease causes the majority of perioperative complications after peripheral vascular surgery. Twenty-four patients with stable coronary disease undergoing peripheral revascularization were studied using continuous electrocardiographic monitoring to determine the incidence of perioperative asymptomatic myocardial ischemia and its relation to postoperative clinical ischemic events. Patients were monitored preoperatively (17 +/- 1 hours), intraoperatively and postoperatively (29 +/- 2 hours) using 4-channel calibrated amplitude-modulated units. Fifteen patients (63%) had early postoperative silent ischemia; 3 also had preoperative silent ischemia and 5 intraoperative transient ischemia. Patients with and without silent ischemia had similar clinical characteristics, perioperative antianginal medications and postoperative episodes of hemodynamic instability. However, 8 of 15 patients (53%) with silent ischemia had postoperative clinical ischemic events (2 had myocardial infarction, 2 had new congestive heart failure and 4 had new rest angina), versus only 1 of 9 patients (11%) without silent ischemia who had angina (p less than 0.05). Early postoperative silent myocardial ischemia occurs frequently after vascular surgery and is associated with postoperative clinical ischemic events.

Aged↗
PubMed1989

Acute effects of carbon monoxide exposure on individuals with coronary artery disease.

The purpose of this study was to determine, using more objective evidence than that reported in previous studies, whether or not exposures to carbon monoxide that produce approximately 2% or 4% blood carboxyhemoglobin levels cause an exacerbation of myocardial ischemia during a progressive exercise test. The objective measurements were based on the development of electrocardiographic evidence of ischemia. In addition, time to onset of angina pectoris was studied. Male subjects, ages 35 to 75, with stable exertional angina pectoris and positive exercise treadmill tests with reproducible ischemic ST-segment changes in their electrocardiograms, were studied. In addition, each subject fulfilled at least one of the following criteria of coronary artery disease: angiographic evidence of at least a 70% occlusion of one or more major coronary artery; prior documented myocardial infarction; or a positive exercise thallium test. Each subject was evaluated on four separate occasions, a qualifying visit and three blinded test visits, which involved exposure (in random order) to air without added carbon monoxide and to air that contained carbon monoxide concentrations calculated to produce approximately 2.2% or 4.4% carboxyhemoglobin, measured by gas chromatography, at the end of the exposure period. These immediate postexposure target levels were set 10% higher than the desired postexercise carboxyhemoglobin levels of 2.0% and 4.0% because exercise while breathing room air results in loss of carbon monoxide. The actual one-minute postexercise levels reached were 2.0% +/- 0.1% (mean +/- standard error of the mean) and 3.9% +/- 0.1%. On each test day, the subject performed a symptom-limited exercise test on a treadmill, was exposed for approximately one hour to air or to one of two levels of carbon monoxide in air, and then performed a second exercise test. Time to the onset of ischemic ST-segment changes and time to the onset of angina were determined for each exercise test. The percent difference for these endpoints on the pre- and postexposure exercise tests was determined, and then the results on the 2%-COHb-target day and the results on the 4%-COHb-target day were compared to those on the control day. Data from the 63 subjects who completed the three test visits and met all protocol criteria were analyzed. There were 5.1% (p = 0.01) and 12.1% (p less than or equal to 0.0001) (trimmed mean) decreases in the time to development of ischemic ST-segment changes after the 2%- and 4%-COHb-target exposures, respectively, compared to the control day.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Silent ischemia on Holter monitoring predicts mortality in high-risk postinfarction patients.

The relative prognostic significance of ischemic ST changes on two-lead continuous electrocardiographic (Holter) monitoring in 103 high-risk postinfarction patients was examined. Ischemic ST changes were detected in 30 patients, with a median number of five episodes per day and median total daily duration of 157 minutes. Only one third of these patients reported any angina in the hospital, and 28 of the 30 patients had silent ST changes on Holter monitoring. The remaining 73 patients had no ischemic ST changes on Holter monitoring. At one year, nine (30%) of 30 patients with ischemic ST changes were dead vs only eight (11%) of 73 patients without such changes. Multivariate Cox's hazard function analysis on 18 variables, including age, type of infarction, Lown and Killip class, ejection fraction, and medications, showed that the presence of ST changes on Holter monitoring was a significant predictive variable for one-year mortality in the overall study population and particularly in the subgroup of 59 patients who could not undergo early exercise treadmill testing. Thus, ischemic ST changes on Holter monitoring, the majority of which are silent, occur in nearly one third of high-risk postinfarction patients and are significantly associated with one-year mortality.

Actuarial Analysis↗
PubMed1988

Death after acute myocardial infarction: interrelation between left ventricular dysfunction, arrhythmias and ischemia.

Patients who survive an acute myocardial infarction face an increased risk of sudden death for approximately 6 months after hospital discharge; their prognosis is determined by the severity of their coronary arteriosclerosis and the degree of left ventricular dysfunction. Frequent ventricular premature complexes and evidence of ischemia either spontaneously or on treadmill are also markers for early morbidity and mortality in patients who are discharged from the hospital after acute myocardial infarction. The degree of left ventricular dysfunction is the strongest predictor of mortality; patients who have both left ventricular dysfunction, frequent premature ventricular beats and evidence of ischemia are at the highest risk of mortality after hospital discharge. It appears likely that all 3 of these risk factors interact and that therapy to reduce morbidity and mortality after myocardial infarction should aim at the amelioration of each of these risk factors. A model for the interaction of these risk factors is proposed and an approach to treatment for patients at high risk of mortality after hospital discharge after myocardial infarction is suggested.

Arrhythmias, Cardiac↗
PubMed1988

Circadian patterns of myocardial ischemia: pathophysiologic and therapeutic considerations.

Recent evidence suggests that acute myocardial infarctions tend to occur most frequently in the early morning hours after awakening. In addition, the peak time of occurrence of out-of-hospital sudden death is during the same morning period, which suggests that the pathophysiologic factors influencing these acute ischemic and arrhythmic events may be similar. Although it is clear that arising from sleep is associated with an increased heart rate and blood pressure, two important determinants of myocardial oxygen demands, other factors may be responsible for a paradoxical decrease of coronary blood flow at the same time. It is possible that vascular receptor sensitivity may vary or that the early morning hours may be associated with a hyperaggregability of platelets; this would provide an additional pathophysiologic explanation for ischemic events related to platelet aggregation and coronary thrombosis, which are known to play a central role in the initiation of unstable angina, acute infarction, and sudden death. An understanding of the circadian pattern of ischemic events may be a guide for future therapeutic interventions during this period. Studies suggest that use of medications that provide continuous antiischemic activity throughout the 24-h day should be considered.

Circadian Rhythm↗
PubMed1988

Nifedipine in acute myocardial infarction: an assessment of left ventricular function, infarct size, and infarct expansion. A double blind, randomised, placebo controlled trial.

The influence of nifedipine on left ventricular ejection fraction, infarct size, and infarct expansion was studied in a prospective, double blind, randomised, placebo controlled trial in 132 patients with low risk acute myocardial infarction of less than 12 hours duration, defined by an initial left ventricular ejection fraction greater than 35% and clinical Killip class of less than or equal to II. Sixty four patients were assigned to nifedipine 120 mg/day and 68 to placebo. Treatment was started on average (SEM) 8.0 (0.2) hours after onset of pain and continued for six weeks. Gated blood pool scans, thallium scans, and cross sectional echocardiograms were performed before treatment and at 10 days. There were no significant differences between the two groups in age, sex, cardiac risk factors, or use of other medications. Mean (SEM) global left ventricular ejection fraction was not different before treatment (nifedipine group 53 (2%), placebo group 55 (2%) and did not differ at 10 days (nifedipine group 54 (2%), placebo group 52 (2%). There were also no differences in regional wall motion or regional ejection fractions. Thallium defects quantified by computer analysis were similar in both groups before treatment (nifedipine 7.8 (0.7), placebo 7.9 (0.7)) and at 10 days (nifedipine 5.3 (0.7) placebo 5.3 (0.7)). In the subgroup of patients with transmural infarction who had good quality echocardiograms and serial studies (n = 30), there was no difference in mean (SEM) baseline infarct segment lengths between the two groups (nifedipine 70 (4) mm, placebo 65 (4) mm); however, the nifedipine group demonstrated no significant change in infarct segment length between the initial and 10 day studies ( + 0.6 (3) mm) while there was a significant increase in the infarct segment length in the placebo group (+ 7.8 (4) mm). The infarct segment length increased by >/= 1 cm in seven (47%) placebo patients but in only one (7%) nifedipine patient. The nifedipine group had a significant initial 10% decrease in mean arterial pressure whereas there was no change in the in the placebo group; this blood pressure difference persisted for 10 days. Thus although the early administration of nifedipine has no detectable effect on clinical outcome and infarction size, it may reduce early infarct expansion via an afterload reduction mechanism in patients with transmural infarction. These initial results must be interpreted with caution and need to be confirmed in a larger trial.

Adult↗
PubMed1988

Double vs single balloon technique for aortic balloon valvuloplasty.

Percutaneous aortic valvuloplasty using a single dilating balloon has been associated with significant but modest reduction in transvalvular pressure gradient and increase in valve area. The balloon diameter is usually 20 mm or smaller to avoid disruption of aortic root structure and to permit forward blood flow during inflation. To evaluate the safety and efficacy of valvuloplasty using a combination of balloons with larger maximum inflated diameters, we compared results of aortic valvuloplasty in 21 patients using either the single or double balloon technique. Mean maximum inflated balloon diameter was 19.4 mm +/- 1.4 for the single balloon technique, while the mean sum of diameters for the simultaneous double balloon technique was 36.3 mm +/- 3.9. The mean age, aortic annulus diameter, and predilatation aortic valve area were not different among groups. Mean aortic transvalvular gradient reduction and mean aortic valve area increase were greater for the double balloon technique. The procedure was well tolerated with no major complications. No change in the degree of aortic regurgitation was noted. The double balloon technique for aortic valvuloplasty is safe and more effective at improving aortic valve area and transvalvular gradient than the conventional single balloon technique.

Aged↗