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Biomedical subjects

R L Feldman

Publications and source records attributed to R L Feldman.

At least 37 records · Page 2Linked to original sources
PubMed1988

Contrast media-related complications during cardiac catheterization using Hexabrix or Renografin in high-risk patients.

Contrast media may lead to adverse reactions during cardiac catheterization. Hexabrix has less hemodynamic and electrophysiologic effects than Renografin-76. To assess relative complication rates using these agents, 82 patients with heart failure or "unstable" ischemic syndromes and undergoing catheterization were prospectively randomized to receive either Hexabrix or Renografin. Clinical diagnoses, hemodynamics before contrast media administration, left ventricular ejection fraction, case duration, contrast volume and cine film quality were similar in the 2 groups. The condition of 1 patient assigned to receive Renografin was deemed too unstable and Hexabrix was safely used. In the other patients, a total of 17 adverse reactions occurred (7 before administration of contrast and thus unrelated: 4 Hexabrix- and 3 Renografin-assigned patients, difference not significant). Three contrast-induced adverse reactions were considered minor (Hexabrix 2, Renografin 1, difference not significant). Severe adverse reactions requiring intervention, such as pulmonary edema and hypotension, were more frequent in patients who received Renografin (6 of 38, 16%) as compared with Hexabrix (1 of 43, 2%) (p less than 0.05). It is concluded that in high-risk patients undergoing cardiac catheterization, Hexabrix is tolerated better than Renografin and should be considered for routine use.

Angiocardiography↗
PubMed1988

Myocardial metabolic and hemodynamic effects of dichloroacetate in coronary artery disease.

Dichloroacetate (DCA), which activates pyruvate dehydrogenase, has the potential to enhance carbohydrate and lactate utilization in animals, but data from patients with coronary artery disease are lacking. Accordingly, 9 patients (ages 49 to 72 years) with angina and coronary artery disease undergoing catheterization were studied. Systemic and coronary hemodynamic and metabolic measurements were made before and during DCA administration (mean dose 35 mg/kg, intravenously). DCA increased left ventricular (LV) stroke volume from 77 +/- 7 to 87 +/- 7 ml and decreased systemic vascular resistance from 1,573 +/- 199 to 1,319 +/- 180 dynes.s.cm-5 (both, p less than 0.01). There were no significant changes in heart rate, mean aortic pressure, LV end-diastolic pressure, LV dP/dt max, coronary sinus flow, coronary resistance or myocardial oxygen consumption, but myocardial efficiency index (LV work/myocardial oxygen consumption) improved from 24 to 32% (p less than 0.05). Myocardial lactate consumption was maintained (21 +/- 8 vs 19 +/- 11 X 10(-3) mEq/min, p is not significant at p less than or equal to 0.05 level) at a lower arterial lactate concentration (0.72 +/- 0.09 to 0.47 +/- 0.08 mEq/liter, p less than 0.05). DCA appears to stimulate myocardial lactate utilization at a lower arterial concentration, cause peripheral vasodilation, augment stroke volume and enhance myocardial efficiency in patients with coronary artery disease.

Acetates↗
PubMed1988

Systemic and coronary hemodynamic effects of combined oral alpha- and beta-adrenergic blockade (labetalol) in normotensive patients with stable angina pectoris and positive exercise stress tests.

The systemic and coronary hemodynamic effects of combined alpha- and beta-adrenergic blockade produced by oral labetalol were assessed in 12 normotensive patients with angina pectoris and an ischemic electrocardiographic response to exercise stress. At rest, labetalol (200 mg, orally) produced systemic vasodilation (systemic vascular resistance -9%, p less than .01) as aortic pressure fell and cardiac output was unchanged. Left ventricular (LV) end-diastolic pressure also fell slightly (17%, p = .05). Systemic vasodilation was not accompanied by reflexly mediated increases in heart rate. Coronary flow and resistance and myocardial oxygen uptake were unchanged. Before labetalol, supine bicycle exercise produced angina in 10 patients. After labetalol, exercise duration was prolonged in 6 of these 10 (average 56%). During exercise, tachycardia was blunted (-7%, p less than .05) as were increases in aortic pressure (-12%, p less than .01) and coronary sinus flow (-25%, p = .03). Cardiac output and LV end-diastolic pressure were similar to control period values. These hemodynamic effects of oral labetalol appeared beneficial, differed from those expected of classic beta-adrenergic blocking agents, and were, in general, similar to those we have observed after intravenous labetalol. The clinical response was good and the drug safe. Labetalol should undergo further evaluation in normotensive as well as hypertensive patients with ischemic heart disease.

Administration, Oral↗
PubMed1988

Coronary artery spasm and its relationship to exercise in patients without severe coronary obstructive disease.

Coronary artery spasm is reported to occur with exercise. In patients without severe coronary atherosclerosis, the evidence for exercise-induced coronary artery spasm is limited. Three patients with positive exercise tests but no severe coronary atherosclerosis are presented. Coronary artery spasm was provoked and verified by angiography in all three, but coronary angiography during exercise failed to demonstrate spasm. The literature is reviewed and the value of a routine protocol for evaluation is discussed.

Adult↗
PubMed1988

Systemic and coronary hemodynamics of labetalol in normotensive patients with ischemic heart disease.

The systemic and coronary hemodynamic effects of combined alpha- and beta-adrenergic blockade produced by labetalol were assessed in 24 normotensive patients with angina pectoris and an ischemic electrocardiographic response to exercise stress. Both the intravenous (0.5 mg/kg) and oral (200 mg) formulations of labetalol were evaluated. At rest, labetalol produced systemic vasodilation (systemic vascular resistance -16% after intravenous and -8% after oral labetalol, both p less than 0.05) without change in heart rate. Aortic pressure usually was lower and cardiac output preserved or increased. Left ventricular end-diastolic pressure was unchanged. Coronary sinus flow was usually unchanged after either route of administration. Exercise duration was prolonged in 14 of the 20 patients with severe coronary artery disease. During exercise, tachycardia was blunted (-12% after intravenous, -7% after oral labetalol, both p less than 0.05) as was the increase in mean aortic pressure (-12% and -13% intravenous and oral labetalol respectively, both p less than 0.05), left ventricular end-diastolic pressure [-7% and -1%, respectively, both p = not significant (NS)] was unchanged. Coronary sinus flow (-16% and -25%, respectively, both p less than 0.05) was decreased as heart rate and aortic pressure were lower. Cardiac output, systemic vascular resistance, and coronary vascular resistance were similar to control exercise. The hemodynamic effects of intravenous and oral labetalol are, in general, similar. Hemodynamic responses differ from those produced by other beta-blockers and by calcium antagonists.

Coronary Circulation↗
PubMed1987

Effects of nicardipine on exercise- and pacing-induced myocardial ischemia in angina pectoris.

To define the effects of nicardipine, a new dihydropyridine calcium antagonist drug, on exercise- and pacing-induced myocardial ischemia, 15 men with coronary artery disease were studied during cardiac catheterization. Nicardipine was administered intravenously as a 2-mg bolus followed by an infusion titrated to maintain a 10- to 20-mm Hg decrease in systolic arterial pressure. At rest, nicardipine decreased systemic and coronary vascular resistances, left ventricular end-diastolic pressure and increased coronary blood flow, heart rate and myocardial oxygen consumption. During bicycle exercise-induced myocardial ischemia, nicardipine significantly prolonged exercise duration and time to 1 mm of ST-segment depression. These changes were associated with no alteration in the product of systolic pressure and heart rate, decreased left ventricular end-diastolic pressure, systemic and coronary vascular resistances and increased coronary blood flow, as well as myocardial oxygen consumption. During atrial pacing, the heart rate threshold for myocardial ischemia was not changed by nicardipine administration, despite improvement in the ratio of coronary blood flow to myocardial oxygen consumption and hemodynamic changes otherwise similar to those during exercise. Nicardipine favorably influenced myocardial metabolic state, as indexed by lactate extraction during pacing-induced ischemia. Nicardipine is a potent coronary and systemic vasodilating drug that improves exercise tolerance and myocardial metabolic response to pacing stress, the mechanism for which appears to be partially mediated through increased coronary blood flow.

Angina Pectoris↗
PubMed1987

Comparison of selective (beta 1) and nonselective (beta 1 and beta 2) beta-adrenergic blockade on systemic and coronary hemodynamic findings in angina pectoris.

To investigate the influence of selective beta 1-adrenergic blockade, in contrast to beta 1- and beta 2-adrenergic blockade, systemic and coronary hemodynamics were studied. Measurements were made at rest and during exercise in 23 patients with suspected coronary artery disease (CAD) before and after either metoprolol or propranolol, given in doses to provide comparable beta 1-receptor blockade. Quantitative coronary angiography was performed at rest. Using a randomized, double-blind protocol, either beta 1 and beta 2 blockade was produced by propranolol (0.1 mg/kg intravenously), or selective beta 1 blockade was produced by metoprolol (0.15 mg/kg intravenously). As expected, at these doses both drugs produced a comparable decrease in heart rate at rest and during exercise, averaging 9% and 14% after propranolol and 10% and 16% after metoprolol. Exercise duration to ischemia was prolonged in most patients with severe CAD after either propranolol (5 of 7) or metoprolol (6 of 10) treatment. The effects of these 2 beta-blocking drugs on systemic hemodynamic values at rest and during exercise were similar. Additionally, coronary sinus flow was usually unchanged by both drugs at rest (-5% after propranolol and -4% after metoprolol, differences not significant) and decreased a similar amount during exercise (-15% after propranolol and -9% after metoprolol, both p less than 0.05). Coronary resistance did not change significantly with either drug (0% after propranolol and 3% after metoprolol), and during exercise (11% after propranolol and 3% after metoprolol), suggesting that decreases in flow were secondary to reduced demand. Furthermore, neither drug produced detectable changes in coronary artery size.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1987

Effect of nicardipine on determinants of myocardial ischemia occurring during acute coronary occlusion produced by percutaneous transluminal coronary angioplasty.

In 10 patients undergoing percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery (LAD), the clinical, electrocardiographic and hemodynamic effects of acute intravenous calcium channel antagonism with nicardipine (2 mg over 1 minute, followed by a constant infusion of 25 to 50 micrograms/min) were assessed during temporary LAD occlusion. Onset of myocardial ischemia during coronary occlusion was prevented or delayed after administration of nicardipine in 7 of the 10 patients. During infusion of nicardipine and during LAD occlusion, residual great cardiac vein blood flow increased in 9 of 10 patients compared with residual flow during occlusion before nicardipine (10%, p less than 0.05). Nicardipine also decreased mean aortic pressure, but was associated with a reflex-mediated increase in heart rate. Overall, the double product, an index of global myocardial oxygen demand, decreased 7% (p less than 0.05). Thus, nicardipine usually diminished ischemia induced by acute transient coronary occlusion by increasing collateral flow while oxygen demand decreased.

Aged↗
PubMed1987

Angiographic morphology of restenosis after percutaneous transluminal coronary angioplasty.

Restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) occurs frequently. To better define the restenosis process, a quantitative analysis was performed of coronary angiographic morphologic characteristics at restenosis, before and immediately after PTCA. In 22 patients cine frames showing stenosis at its most severe narrowing were traced and quantitatively analyzed. Immediately after PTCA, stenosis diameter (0.7 +/- 0.3 to 1.9 +/- 0.6 mm, mean +/- standard deviation, p less than 0.05) was increased; percent stenosis (77 +/- 11 to 34 +/- 16%, p less than 0.05), neck index (1.2 +/- 1.4 to 0.5 +/- 0.6, p less than 0.05) and irregularity (9 of 22 patients) were decreased. At follow-up, quantitative coronary morphologic values in most cases were similar to those before PTCA. There were individual changes, which occurred in an unpredictable and highly variable fashion, so that average values were not changed. The eccentricity ratio was not significantly changed by angioplasty or at restenosis. Thus, although successful PTCA results in specific changes in angiographic coronary stenotic morphology, these are reversed by the restenosis process.

Angioplasty, Balloon↗
PubMed1987

Systemic and coronary hemodynamic effects of combined alpha- and beta-adrenergic blockade (labetalol) in normotensive patients with stable angina pectoris and positive exercise stress test responses.

The systemic and coronary hemodynamic effects of combined alpha- and beta-adrenergic blockade produced by labetalol were assessed in 12 normotensive patients with angina pectoris and an ischemic electrocardiographic response to exercise stress. When given to the patient at rest, labetalol (0.5 mg/kg intravenously) produced systemic and coronary vasodilation (mean 16% and 13%, respectively, both p less than 0.05); aortic pressure decreased, cardiac output increased and coronary flow and heart rate did not change. Before labetalol treatment, supine bicycle exercise produced angina in all patients. After treatment, exercise duration was prolonged in 8 patients (average 33%). At the same duration of exercise that led to angina during the control period, ST depression in lead V5 was less after labetalol (from 1.2 to 0.4 mm, p less than 0.5). During exercise, tachycardia was blunted (-12%, p less than 0.05) as were the increases in aortic pressure (-12%, p less than 0.05), left ventricular end-diastolic pressure (-7%, difference not significant) and coronary sinus flow (-16%, p less than 0.05). Cardiac output and systemic and coronary vascular resistance were similar to values during control exercise. The hemodynamic effects of labetalol appeared to be beneficial and differed from those of classic beta-adrenergic blocking agents.

Adrenergic alpha-Antagonists↗
PubMed1987

Systemic and coronary hemodynamic effects of combined intravenous diltiazem and nitroglycerin administration.

This study evaluated left ventricular (LV) and coronary hemodynamic effects of intravenous nitroglycerin (NTG) in the presence of an intravenous infusion of diltiazem in 15 patients with severe coronary disease. Diltiazem (250 microgram/kg bolus followed by 1.4 micrograms/kg/min infusion) alone decreased mean systemic blood pressure (mean 6%) without changing heart rate or LV end-diastolic pressure. The rate of rise in LV pressure declined slightly (4%), and peripheral resistance decreased (19%). Coronary sinus (CS) and great cardiac vein (GCV) flows were preserved. Addition of NTG (average, 68 micrograms/min) decreased systemic pressure further (7%) as LV end-diastolic pressure declined (5 mm Hg). These pressure changes were accompanied by a 10% increase in heart rate (compared with the heart rate found with diltiazem alone). Peripheral resistance was similar to values after diltiazem alone. The CS and GCV flows did not decrease. The sequence of intravenous drug administration was reversed in three other patients with combination therapy, producing similar effects, regardless of which drug was administered first. Hemodynamic effects of intravenous diltiazem alone and its combination with intravenous NTG seemed potentially favorable for patients with ischemic heart disease.

Adult↗
PubMed1987

Comparison of diltiazem and nifedipine alone and in combination in patients with coronary artery spasm.

Fifteen patients with coronary artery spasm completed a double-blind placebo-controlled trial comparing diltiazem and nifedipine. Increasingly, higher daily doses (diltiazem, 90 to 360 mg; nifedipine, 30 to 120 mg) were administered to achieve optimal clinical effects. Daily diaries and ambulatory electrocardiographic recordings were used to assess efficacy and side effects. Both drugs significantly decreased angina frequency compared with that in the preceding placebo period (diltiazem 1.4 +/- 0.4 [mean +/- SEM] to 0.4 +/- 0.2 episodes per day; nifedipine 1.4 +/- 0.3 to 0.4 +/- 0.1 episodes per day; both p less than 0.05). Ambulatory electrocardiographic recordings showed fewer ST shifts than were expected during all treatment periods (0.02/h recorded during placebo, none during diltiazem and 0.02/h during nifedipine therapy). Although some patients responded better to one drug than the other, neither drug resulted in a clearly superior clinical response. Diltiazem was discontinued in one patient because of urticaria, but the total number of side effects was higher with nifedipine (12 of 15 patients) than with diltiazem (5 of 15, p less than 0.01). Nine patients remained symptomatic on single drug treatment and entered open label treatment with the combination of diltiazem and nifedipine. Three patients did not tolerate the combination because of important side effects; the other six also had side effects, but these were relatively minor. Four patients received no more benefit from the combination than from a single agent; the condition of two patients improved. Both diltiazem and nifedipine provide effective antianginal therapy for coronary spasm, but diltiazem has fewer side effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

A review of medical therapy for coronary artery spasm.

This article reviews controlled trials of medical therapy for coronary artery spasm. The calcium antagonists, either alone or in combination with long-acting nitrates, are effective therapy for patients with coronary artery spasm. These drugs definitely decrease angina and the frequency of ischemic ST shifts recorded during continuous electrocardiographic monitoring. Therapy is still relatively nonspecific, however, since the mechanism(s) that lead to spasm remain unknown. Interestingly, the initial response to therapy is similar regardless of the presence or absence of severe coronary artery disease accompanying spasm. Drugs that block adrenergic or serotonin receptors or that alter platelet aggregability or prostaglandin production have been ineffective in relieving angina or decreasing the frequency of ischemic ST shifts. Patients with resting angina syndromes are a heterogeneous group; many do not have coronary spasm since other mechanisms also precipitate ischemic episodes at rest. Prevention of angina or ischemic ST shifts may not necessarily prevent acute myocardial infarction and sudden cardiac death. Both initial and long-term therapies should be individualized according to a detailed clinical and angiographic assessments of each patient.

Adrenergic beta-Antagonists↗
PubMed1986

Left ventricular dyskinesia reversed by intravenous nitroglycerin: a manifestation of silent myocardial ischemia.

Patients with coronary artery disease (CAD) frequently have left ventricular (LV) wall motion abnormalities in the absence of symptoms. Thirty-one patients with such LV wall motion abnormalities in the absence of symptoms participated in a study of the response of these abnormalities to ascending doses of intravenous nitroglycerin (NTG). In a subgroup of 20 patients the relation between the location of LV wall motion abnormalities and the presence or absence of significant CAD (greater than or equal to 50% diameter reduction), in the vessel supplying the LV region, was assessed. Wall motion improved after intravenous NTG; the ejection fraction increased by 3.7% (mean p less than 0.05) and by 9.4% in the 19 patients who responded. There was no significant increase in heart rate; both LV systolic and end-diastolic pressures decreased minimally (12.5 and 3.5 mm Hg, respectively, p less than 0.05). The ejection fraction response was observed with NTG doses less than or equal to 200 micrograms and no dose-response relation was apparent. In the subgroup subjected to regional wall motion analysis, the presence of dyskinesia was significantly (p = 0.007) associated with the presence of important CAD in a vessel supplying that region. Further, the fact that wall motion improvement after NTG was significantly (p = 0.002) associated supports the concept that silent ischemia results in LV regional wall motion abnormalities, which can be reversed with low dose intravenous NTG.

Adult↗