Search PubMed⌕ Search

Biomedical subjects

R L Feldman

Publications and source records attributed to R L Feldman.

At least 91 records · Page 5Linked to original sources
PubMed1984

Thromboxane release in coronary artery disease: spontaneous versus pacing-induced angina.

To determine thromboxane A2 release in coronary artery disease, we measured its stable metabolite thromboxane B2 by radioimmunoassay in 20 patients. In 15 patients with stable disease (last angina episode greater than 96 hours before study), coronary venous thromboxane B2 concentrations were lower than in aortic blood (mean 109 +/- 36 vs 194 +/- 40 pg/ml, p less than 0.001). In contrast, in five other patients with spontaneous angina, coronary venous thromboxane B2 concentrations were higher than aortic thromboxane B2 concentrations during the angina episode (mean 1716 +/- 316 vs 875 +/- 388 pg/ml, p less than 0.02). Plasma thromboxane B2 levels were in the normal range (mean 175 +/- 35 pg/ml) in patients with stable angina but significantly (p less than 0.02) higher in patients with spontaneous angina. With atrial pacing to the point of chest pain and/or ECG changes in patients with stable coronary artery disease, aortic thromboxane B2 concentrations increased in 10 of 13 patients (mean 283 +/- 70 pg/ml, p less than 0.02). Coronary venous thromboxane B2 concentrations increased in seven patients at peak pacing rates (mean 223 +/- 76 pg/ml) and in three other patients after termination of pacing. These data indicate that release of thromboxane A2 is much greater during spontaneous angina than with pacing stress in patients with coronary artery disease. Thromboxane A2 released during spontaneous or pacing-induced angina may modulate coronary and systemic vascular tone. Enhanced thromboxane A2 activity may either precede or follow myocardial ischemia and could be a factor in the initiation and propagation of the ischemic episode.

Adult↗
PubMed1984

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.

Angina Pectoris, Variant↗
PubMed1984

Comprehensive drug management of angina pectoris.

Our current understanding of the pathophysiology of angina and myocardial ischemia includes both anatomic and dynamic mechanisms. The relative contribution made by hemodynamically important atherosclerotic obstruction and dynamic coronary artery obstruction, either by arterial spasm or arteriolar constriction, to the pathophysiology of ischemia in any given patient should be delineated. This information appears to be useful in identifying patients likely to achieve major benefit from vasodilators on the one hand or beta-adrenergic blocking agents on the other. A number of agents are now available within these two pharmacologic classes. There are some differences in action of these various agents that require thorough familiarity of effects of these drugs so that their action can be optimized. Practically speaking, the large majority of patients with an angina syndrome will respond to nitrates. Nitrates are extremely safe and cheap; thus, their use for relief or prevention of the acute ischemic episode remains the initial treatment of choice. When symptoms are more than mild to moderate in severity, or unacceptably controlled in frequency using nitrates alone, other pharmacologic measures are needed (Fig. 2). In patients with a predominant symptom of effort angina, suggesting that a hemodynamically important atherosclerotic-type obstruction is responsible for the syndrome, beta-adrenergic blocking drugs can be very helpful. If effort angina remains unacceptably controlled or adverse effects occur, a calcium-channel antagonist may be added or substituted. These latter agents do not exacerbate bronchospasm or peripheral vascular disease, and they offer a distinct advantage over beta-adrenergic blocking agents in patients with angina who have such disorders. Where the predominant symptom is rest angina, or the patient has other evidence suggesting coronary spasm or arteriolar vasoconstriction, a calcium-channel antagonist may result in a very favorable response. This therapy should be extended not only to patients in whom coronary spasm occurs spontaneously but to those in whom it can be provoked by stimuli such as effort or cold. When spasm is superimposed upon hemodynamically important atherosclerotic obstruction, the favorable response does not seem to be as great as that seen when spasm exists alone. In these cases, coronary bypass surgery, plexectomy , and other nonpharmacologic approaches may have to be added to the pharmacologic regimen.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1983

Comparison of coronary hemodynamic effects of nitroprusside and sublingual nitroglycerin with anterior descending coronary arterial occlusion.

This study compares the coronary hemodynamic effects of an infusion of nitroprusside and of sublingual nitroglycerin in the same patients. The coronary hemodynamic responses of the anterior left ventricular (LV) region to both drugs were studied in 9 patients whose anterior descending branch of the left coronary artery was filled by collaterals. Before and during administration of each drug (given in doses designed to produce similar changes in LV diastolic pressure), heart rate, LV and aortic pressure, and anterior regional flow, oxygen delivery and lactate metabolism were measured. Given in this manner, as expected, both drugs decreased the double product of heart rate and systolic pressure. Concomitant with these changes, anterior regional blood flow increased or decreased modest amounts or did not change with either drug. Similar directional flow changes or no change occurred in 6 patients and directionally different changes in the other 3 patients. The ratio of mean aortic pressure or of the double product to anterior regional flow consistently decreased during the administration of both drugs. Additionally, anterior regional myocardial oxygen uptake remained similar during both drug periods compared with control values. Anterior region lactate extraction was abnormal (less than 10%) in 4 of the 9 patients during the initial control period. Lactate extraction was usually normal during both the nitroprusside and the nitroglycerin periods. In general, coronary hemodynamic values were remarkably similar during both of these periods. Thus, although relative differences in systemic arterial and venous dilation were obtained with nitroprusside and nitroglycerin, similar and beneficial coronary hemodynamic changes generally occurred.

Aged↗
PubMed1983

Systemic, pulmonary, and coronary hemodynamic effects of labetalol in hypertensive subjects.

Long-term therapy with oral labetalol, an alpha- and beta-blocking agent, has been shown to effectively lower blood pressure and heart rate without decreasing cardiac output. We examined the hemodynamic effects of the acute intravenous administration of labetalol in nine hypertensive patients. Labetalol (0.6 +/- 0.1 mg/kg) promptly reduced arterial pressure, heart rate, and systemic vascular resistance without change in stroke volume. Heart rate responses to passive tilt and the Valsalva maneuver were significantly blunted. With isometric exercise, heart rate and mean arterial pressure increased significantly during labetalol therapy but less than in the pre-labetalol phase. In eight patients oral labetalol therapy was continued for six weeks (mean dose 1,050 +/- 105 mg/day), and hemodynamic evaluation was repeated. During oral labetalol therapy, decreases in arterial pressure and heart rate were sustained. Systemic vascular resistance was reduced in five of the eight patients. Hemodynamic responses to tilt, Valsalva maneuver, and handgrip were similar to those during intravenous administration. Coronary blood flow decreased, but coronary as well as pulmonary vascular resistances were unchanged. These data show the efficacy of intravenously administered labetalol in lowering blood pressure and systemic vascular resistance promptly. With long-term oral therapy, decreases in blood pressure are sustained. Labetalol does not appear to have significant effects on pulmonary or coronary vascular resistances.

Adult↗
PubMed1983

Effect of glyceryl trinitrate on coronary and systemic hemodynamics in man.

The effects of sublingual and intracoronary nitrates on coronary artery diameter were evaluated in five separate experiments in man. The first three are concerned with sublingual nitrates and the last two with intracoronary nitrates. The data obtained indicate that (1) administration of a fixed dose sublingual nitrate results in an increase in percent coronary artery stenosis compared with control measurements; (2) small doses of sublingual nitrates can dilate coronary arteries without a significant reduction in systemic arterial pressure or increase in heart rate; (3) the magnitude of percent coronary artery dilation after a fixed dose of sublingual nitrate is inversely related to the size of the coronary artery, that is, the smaller the coronary artery diameter the greater the relative dilation after administration of sublingual nitrate; (4) fixed dose sublingual nitrate often dilated coronary stenoses, but the more narrow stenoses were less likely to dilate; (5) the optimal dose of intracoronary nitrate required to produce maximal or near maximal coronary dilation without clinically important systemic hemodynamic effects is in the range of 200 micrograms; (6) intracoronary nitrate is a more potent coronary artery dilator than sublingual nifedipine, when administered as a 10 mg dose.

Administration, Oral↗
PubMed1983

Titrates for treatment of unstable angina pectoris and coronary vasospasm.

The treatment of a patient with unstable angina at the time of the initial presentation of the physician can begin with nitrates. The beneficial action of nitrates are several. Nitrates dilate epicardial coronary arteries as well as many coronary artery stenoses. They may be effective because of this action plus a marked effect on decreasing ventricular volume and ventricular end diastolic pressure. Perhaps the best way to manage patients with severe angina that may be in part related to coronary artery vasoconstriction is to combine a long-acting nitrate with a calcium antagonist. The combined use of nitrates and calcium antagonists will (1) dilate the coronary arteries to maintain coronary blood flow, (2) decrease systemic arterial pressure and thus decrease peripheral vascular resistance, and (3) dilate peripheral veins and thus decrease ventricular volume and pressure. When proper doses are used, the combination may be more effective than either drug alone. Of course, proper dosing must be determined for the individual patient by the physician. Initial treatment with the nitrates should begin with small doses and gradually build up. Similar dosing schedules should be used for the calcium antagonists. Both doses can be increased to high levels is the clinical situation warrants it.

Adrenergic beta-Antagonists↗
PubMed1983

Influence of aortic stenosis on the hemodynamic importance of coronary artery narrowing in dogs without left ventricular hypertrophy.

Coronary hemodynamic effects of controlled left ventricular outflow obstruction stimulating aortic valve stenosis were studied in 20 open-chest dogs, with and without graded coronary artery diameter narrowing. Aortic stenosis was regulated so that a mean left ventricular-aortic pressure gradient of 46 +/- 20 mm Hg (mean +/- standard deviation) was created as both heart rate and stroke volume were unchanged. In addition, during aortic stenosis, mean aortic pressure (105 +/- 17 to 84 +/- 15 mm Hg, p less than 0.05) and diastolic pressure time index/systolic pressure time index ratio (1.2 +/- 0.3 to 0.6 +/- 0.2, p less than 0.05) decreased and end-diastolic left ventricular pressure (7 +/- 4 to 14 +/- 6 mm Hg, p less than 0.05) increased. With no coronary narrowing, mean coronary flow increased during aortic stenosis (53 +/- 23 to 62 +/- 23 ml/min) as the percentage of diastolic flow increased (83 +/- 6 to 89 +/- 4) and endocardial/epicardial ratio decreased (1.14 +/- 0.16 to 0.95 +/- 0.24) (all p less than 0.05). Peak reactive hyperemic flow also decreased (168 +/- 85 to 125 +/- 73 ml/min, p less than 0.05). This value with no coronary narrowing was similar to peak hyperemic flow with 60% narrowing without aortic stenosis. With 90% coronary narrowing, mean coronary flow decreased with or without aortic stenosis. Transmural flow distribution also decreased but was lower during aortic stenosis (0.86 +/- 0.19 to 0.61 +/- 0.25, respectively; p less than 0.05). These data suggest that although mean coronary flow is increased during aortic stenosis, endocardial flow may be limited, and coronary reserve exposed during reactive hyperemia appears decreased. When a coronary artery is narrowed, aortic stenosis has an even more important hemodynamic influence on the coronary circulation.

Acute Disease↗
PubMed1983

Quantitative coronary angiography during intracoronary streptokinase in acute myocardial infarction: how long to continue thrombolytic therapy?

An intracoronary infusion of streptokinase is often administered in patients with acute myocardial infarction. To address the question of how long intracoronary streptokinase should be infused, we studied 13 patients with symptoms and electrocardiographic findings suggesting an evolving myocardial infarction. We used subselective catheterization techniques and made quantitative angiographic measurements of the percentage of reduction of coronary artery (CA) diameter before intracoronary streptokinase therapy, immediately after reperfusion was established, and at the completion of streptokinase infusion. Before intracoronary streptokinase and after intracoronary nitroglycerin, nine patients had 100% obstruction of the CA in the "infarct-related vessel." In seven patients reperfusion was established (25 +/- 21 min, mean +/- SD) at which time CA diameter was reduced by 77 +/- 22%. The streptokinase infusion was then continued until repeated films (every 10 to 15 min) suggested no further change at the site of CA obstruction (93 +/- 68 min). The percentage of CA diameter reduction when streptokinase infusion was discontinued was 55 +/- 32%; this value was less (P less than 0.05) than that observed early after reperfusion. These data show that after initial reperfusion was achieved by the use of intracoronary streptokinase, additional streptokinase lessened the reduction of CA diameter. Residual thrombus may be present at the narrowed CA site early after reperfusion, and further "cleanup" can be achieved by prolonging streptokinase infusion.

Adult↗
PubMed1983

Comparison of the effects of nitroprusside and nitroglycerin on coronary size.

Nitroglycerin and nitroprusside are known to differ in their relative degree of systemic arterial and venous dilation. Nitroglycerin has been shown to be a potent large-vessel coronary dilator, but the effects of nitroprusside on coronary artery size are unclear. Accordingly, we studied coronary artery angiographic responses to both nitroprusside and nitroglycerin in 12 patients. Diameters Of left coronary artery segments were measured by quantitative angiography before and during an intravenous infusion of nitroprusside and after sublingual nitroglycerin when both drugs were administered in doses adjusted to achieve reductions in aortic pressure. Dilation of the left coronary artery was observed after nitroprusside and after nitroglycerin. Degrees of dilation were similar in the various left coronary artery segments after either nitroprusside or nitroglycerin. In general, segments located more proximally dilated less than those located more distally after either agent. We conclude that both nitroprusside and nitroglycerin are potent dilators of large epicardial and of smaller intramuscular coronary artery segments. The magnitude of dilation of all measured left coronary artery segments appeared remarkably similar with nitroprusside and nitroglycerin given in doses that produced a similar reduction in aortic pressure.

Angiography↗
PubMed1983

Electrocardiographic changes with coronary artery spasm.

The presence or absence of important ECG changes (e.g., ST elevation or depression greater than or equal to 1 mm) was evaluated in 79 consecutive patients with coronary artery spasm. In eight of these patients ECG changes usually did not accompany episodes of rest angina. Evaluation before, during, and after cardiac catheterization included multiple ECGs and ambulatory monitoring during angina. Our observations suggest that the ECG may not always be a sensitive indicator of coronary spasm. Thus the diagnosis of transient myocardial ischemia secondary to coronary spasm should not necessarily be excluded because of a lack of ECG changes during rest angina.

Aged↗
PubMed1983

Clinical outcome after treatment of rest angina with calcium blockers: comparative experience during the initial year of therapy with diltiazem, nifedipine, and verapamil.

The clinical outcome after the initial year of therapy with either diltiazem (D), nifedipine (N), or verapamil (V) was examined in 45 patients with rest angina. Age, frequency of angina, duration of symptoms, and ejection fraction were similar in all three treatment groups. Coronary artery disease was present in 60% of patients (5 of 13 given D, 8 of 16 given N, and 14 of 16 given V). Coronary spasm was suspected (ST elevation with angina) or documented (angiographically) in 35 (78%) patients. Twenty-nine (64%) patients had greater than 50% decrease in angina without a coronary event (9 taking D, 11 taking N, and 9 taking V). Coronary events (sudden death, infarction, and hospitalization for unacceptable angina control or bypass surgery) occurred in 13 (29%) patients (two taking D, four taking N, and seven taking V). To achieve these responses, 20 (44%) patients required additional antianginal drugs (long-acting nitrates, beta blockers, or other calcium blockers). Four of these 20 patients were taking D, nine were taking N, and seven were taking V. Seventeen (38%) patients experienced a side effect (none taking D, 6 taking N, and 11 taking V). Although rest angina can be controlled in the majority of patients during the initial year of treatment with calcium blockers, additional therapy is often required. Furthermore, the clinical course of patients presenting with rest angina remains unpredictable, even during calcium blocker treatment. Morbid events continue to occur, related in part to the extent of coronary artery disease.

Adult↗
PubMed1983

Long-term responses to nifedipine in patients with coronary spasm who have an initial favorable response.

Twenty-six patients with angina and coronary spasm participated in a randomized crossover trial comparing nifedipine with isosorbide dinitrate. Eighteen patients had a short-term beneficial response to nifedipine, and 14 of these were followed up for an average period of 9.4 months. During follow-up study, nifedipine was the primary therapy in these 14 patients, but other drugs were added when clinically necessary to control angina. There was an overall 86% beneficial response rate (greater than 50% decrease in angina frequency). However, 2 patients had a large increase (greater than 10 times) and 4 patients had a slight increase (transient) in angina frequency over the long term compared with the short-term response. The other 8 patients had a similar angina frequency compared with the short-term response. Of the 12 patients with a good response (transient slight increase or no change), 8 (67%) required additional drug therapy to maintain angina control. Nifedipine was discontinued in 2, and the dose was decreased in 3 of the 14 patients because of adverse effects. Three patients had a marked increase in angina at 9, 14, and 3 months, requiring hospitalization; 1 patient had coronary bypass for symptom control. Thus, patients with coronary spasm selected because of a favorable short-term response to nifedipine were effectively treated over the long term with nifedipine; however, additional therapy was often needed to control symptoms. Adverse effects were common, but simple reduction of nifedipine dose usually diminished the unwanted effects of the drug.

Angina Pectoris↗
PubMed1983

Coronary arterial aneurysm formation after balloon angioplasty.

The mechanism of coronary stenosis dilatation by percutaneous transluminal coronary angioplasty (PTCA) is incompletely understood. Five men who developed coronary arterial aneurysms at the site of PTCA are described. All patients were in New York Heart Association functional class III or IV at the time of PTCA. In 2 patients acute myocardial infarction was evolving and both had acute coronary occlusion. The other 3 patients had angiographic evidence of intimal disruption or acute coronary reocclusion as a result of PTCA, one of whom had undergone emergency coronary artery bypass grafting. Three patients received intracoronary streptokinase during PTCA. One patient was asymptomatic and 4 were symptomatic when the aneurysms were identified between 11 days and 4 months after PTCA. Other than the complex course and anatomy of these patients before and immediately after PTCA, no other features distinguished them from others undergoing this procedure.

Aged↗