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Biomedical subjects

R Forman

Publications and source records attributed to R Forman.

At least 55 records · Page 3Linked to original sources
PubMed1984

Thallium-201 accumulation during reperfusion of ischemic myocardium: dependence on regional blood flow rather than viability.

These experiments in dogs were designed to determine whether the use of thallium 201 (TI-201) accumulation in patients during the reperfusion phase after streptokinase lysis of an intracoronary thrombus is a function of coronary blood flow or a function of myocardial viability. The left anterior descending coronary artery was occluded for 60 minutes in open-chest dogs, and the immediate TI-201 accumulation and regional blood flow (MBF) using microspheres was measured in 2 groups: 10 minutes after reperfusion in 9 dogs (group A) and 24 hours after reperfusion in 6 dogs (group B). There was an 80% or greater reduction in MBF in the subendocardium during ischemia in both groups of dogs, and it was inferred that the subendocardium was destined to become necrotic in group A and had become necrotic in group B dogs. The ratio of TI-201 accumulation to MBF in the tissue that had been ischemic was not significantly different from the ratio in normal tissue despite MBF being in the normal range in group A (n = 7, 2 dogs excluded because of reactive hyperemia) and being markedly decreased in group B. Thus, the immediate TI-201 distribution was related to MBF, and caution is recommended in its use to assess myocardial salvage in the early reperfusion phase after streptokinase lysis of intracoronary thrombi. These data suggest that the intramyocardial accumulation of TI-201 is predominantly a passive process and independent of Na-K ATPase.

Animals↗
PubMed1984

The efficacy of quinidine and disopyramide in the maintenance of sinus rhythm after electroconversion from atrial fibrillation. A double-blind study comparing quinidine, disopyramide and placebo.

In order to compare the relative efficacy of quinidine, disopyramide and a placebo in the maintenance of sinus rhythm after cardioversion from atrial fibrillation and in order to examine the incidence of side-effects, 82 patients with continuous atrial fibrillation (duration more than 1 month but less than 3 years) were randomized in a double-blind fashion to receive quinidine, disopyramide or placebo. Six months after cardioversion there was no significant difference between any of the three groups as regards the number of patients remaining in sinus rhythm. The greater distortion of the atrial architecture which occurs in patients with rheumatic mitral valve disease may explain the failure of these anti-arrhythmic agents to prolong the duration of sinus rhythm in this study, in which patients with valvular heart disease comprised 76% of the total group.

Adolescent↗
PubMed1983

Failure of dobutamine to increase exercise capacity despite hemodynamic improvement in severe chronic heart failure.

The acute hemodynamic and metabolic effects of dobutamine administered during exercise were studied in 8 patients with severe chronic heart failure. Exercise was performed on an upright bicycle ergometer using a graded protocol. During exercise performed without administration of dobutamine, exhaustion occurred after 4.5 +/- 1.2 minutes of exercise. The cardiac index increased from 1.61 +/- 0.25 to 2.67 +/- 0.59 liters/min/m2 (p less than 0.001), the arteriovenous oxygen difference from 7.8 +/- 1.7 to 12.5 +/- 2.4 ml/100 ml (p less than 0.001), and oxygen uptake from 7.9 +/- 3.0 to 41.2 +/- 15.7 mg/100 ml (p less than 0.001). During exercise performed with the administration of dobutamine, the cardiac index was significantly greater than during the control state, 3.23 +/- 0.78 versus 2.67 +/- 0.59 liters/min/m2 (p less than 0.001), while the arteriovenous oxygen difference was significantly lower, 11.2 +/- 2.1 vs 12.5 +/- 2.4 ml/100 ml (p less than 0.01). The arterial lactate level was not significantly changed, 45.3 +/- 17.6 versus 41.2 +/- 15.7 mg/100 ml. Although the dobutamine level tended to increase maximal oxygen uptake compared with the control period of exercise, 9.1 +/- 1.2 versus 8.5 +/- 1.4 ml/kg/min (p less than 0.05), it did not significantly increase exercise capacity, 4.8 +/- 1.5 versus 4.5 +/- 1.2 min. Thus administration of dobutamine in patients with severe chronic heart failure increased the cardiac index during maximal exercise but failed to increase exercise capacity. Since arteriovenous oxygen difference is reduced, dobutamine probably increases blood flow to the nonexercising tissues and not to the actively metabolizing muscles.

Cardiac Output↗
PubMed1983

Improvement in exercise capacity despite cardiac deteriora tion: nonivasive assessment of long-term therapy with amrinone in severe heart failure.

Seven patients with severe congestive heart failure (CHF) were treated with oral amrinone for a mean duration of 39 weeks (range 16 to 72). During the first week of therapy, exercise capacity as assessed on a treadmill using the Naughton protocol, increased substantially from 7.6 +/- 4.2 to 12.1 +/- 4.4 minutes (p less than 0.01). At an early period of follow-up (8 to 12 weeks), a further significant increase in exercise capacity to 14.7 +/- 5.0 minutes (p less than 0.05) was demonstrated, while at a later follow-up exercise capacity had decreased to 11.4 +/- 6.8 minutes (p less than 0.05). This was still significantly greater than prior to amrinone therapy (p less than 0.01). Left ventricular ejection fraction was increased from 14 +/- 4 to 19 +/- 4% (p less than 0.05) during the first week of therapy, but was not significantly different from control at the early and late periods of follow-up. Left ventricular end-diastolic dimension index increased from control value of 43 +/- 5 to 47 +/- 7 mm/m2 (p less than 0.01) at the late period of follow-up. Thus long-term amrinone therapy resulted in a substantial improvement in exercise capacity despite a slow, but progressive decline in cardiac performance.

Adult↗
PubMed1983

Long-term therapy with a new cardiotonic agent, WIN 47203: drug-dependent improvement in cardiac performance and progression of the underlying disease.

Seven patients with severe chronic congestive heart failure were treated with a new cardiotonic agent, WIN 47203 (an analog of amrinone), for an average of 7.4 weeks (range 2 to 15). At the initiation of therapy, hemodynamic improvement occurred in all patients as the cardiac index increased from 1.79 +/- 0.39 to 2.30 +/- 0.44 liters/min per m2 (probability [p] less than 0.05) and pulmonary capillary wedge pressure decreased from 24.1 +/- 6.7 to 16.1 +/- 7.8 mm Hg (p less than 0.05). Long-term therapy produced a substantial symptomatic improvement in five of the seven patients. This improvement was fully sustained in two patients and the remaining three experienced a partial return of their symptoms even though the initial hemodynamic improvements at rest remained evident in all seven patients. Withdrawal of WIN 47203 precipitated hemodynamic deterioration in all patients. The cardiac index decreased from 2.25 +/- 0.40 to 1.64 +/- 0.46 liters/min per m2 (p less than 0.05) while the pulmonary capillary wedge pressure increased from 17.1 +/- 7.8 to 23.2 +/- 12.0 mm Hg (p less than 0.05). Stroke volume index after withdrawal was lower than the control level before therapy (17.0 +/- 6.6 versus 20.3 +/- 4.7 ml/m2; p less than 0.05) and pulmonary capillary wedge pressure was similar. During long-term therapy, no undesirable side effects or hematologic changes were observed. Thus, drug-dependent hemodynamic benefits and apparent progression of the underlying cardiac disease were demonstrated during long-term therapy with WIN 47203.

Cardiac Output↗
PubMed1983

Acute myocardial infarct extension into a previously preserved subendocardial region at risk in dogs and patients.

In this study we quantitated the region of preserved myocardium between a subendocardial myocardial infarct (SEMI) and the endocardium in dogs and determined whether this preserved zone was within the region at risk and whether infarct extension could occur in this region. We also evaluated whether a similar subendocardial region exists in patients with SEMI. A 40-minute temporary occlusion of the left anterior descending coronary artery (LAD) in eight dogs resulted in a 35 +/- 5% transmural infarct with 8 +/- 1% subendocardial preservation as assessed by point-counting of the histologic specimens. In vivo perfusion of coronary vessels with Microfil showed that this preserved subendocardial zone was within the region at risk. The preserved subendocardial zone had significantly fewer cell layers in the dogs ventilated with room air than in dogs ventilated with 100% oxygen (8 +/- 4 vs 19 +/- 4, p less than 0.001), which suggests that diffusion from the ventricular cavity was the mechanism of cell preservation. In contrast, the inspired oxygen concentration did not influence the size of the SEMI. Reocclusion of the LAD for 24 hours in an additional eight dogs, 1 week after a SEMI had been created by a 40-minute temporary occlusion, resulted in both subendocardial and subepicardial extension involving 5 +/- % and 29 +/- 9%, respectively, of the transmural myocardium at the infarct center. Subendocardial infarct extension of a similar dimension to that in dogs ventilated on 100% oxygen was observed in postmortem material from eight patients with infarct extension. The preserved layers of subendocardium presumably receive sufficient nutrients from the ventricular cavity to maintain the viability of this region during temporary, but not permanent, reduction of blood supply from the coronary arteries.

Aged↗
PubMed1983

Comparative effect of verapamil and nitroglycerin on collateral blood flow.

The effects of intracoronary verapamil and nitroglycerin on collateral blood flow were compared under conditions where coronary perfusion pressure was held constant with a servopump and the systemic effects of the drugs were minimal. Both drugs were infused into 12 anesthetized dogs after occlusion of the left anterior descending coronary artery (LAD) and regional myocardial blood flow (MBF) was measured using microspheres. Before the LAD occlusion, the myocardium not perfused by the LAD was labeled to permit calculation of the fraction of tissue normally perfused in the LAD samples and corrections for collateral flow. The central ischemic zone contained 2.5 +/- 0.3% normally perfused myocardium and a 4-mm border zone contained 26.8 +/- 4.3% normal myocardium. This border zone contained 10% of the total tissue supplied by the LAD. The MBF in the central ischemic zone increased from 0.101 +/- 0.019 to 0.113 +/- 0.022 ml/min/g after verapamil infusion (NS) and to 0.149 +/- 0.024 ml/min/g after nitroglycerin (p less than 0.01). Uncorrected MBF in the border zone increased significantly after infusion of both verapamil (0.469 +/- 0.085 ml/min/g, p less than 0.01) and nitroglycerin (0.398 +/- 0.056, p less than 0.05). When corrections were made for interdigitating normal tissue in the border zone, only the MBF after nitroglycerin was significantly increased. Thus, nitroglycerin significantly increased the collateral blood flow to ischemic tissue in the central ischemic and border zones, but verapamil did not.

Animals↗
PubMed1982

Long-term amrinone therapy in patients with severe heart failure: drug-dependent hemodynamic benefits despite progression of disease.

Six patients with severe congestive heart failure refractory to conventional therapy, including vasodilators, were treated with oral amrinone for a mean duration of 41 weeks (range 20 to 72 weeks). At initiation of therapy, the cardiac index increased from 1.74 +/- 0.31 to 2.62 +/- 0.52 (mean +/- SD) liters/min/m2 (p less than 0.01) and pulmonary capillary wedge pressure decreased from 26.5 +/- 3.5 to 19.5 +/- 5.4 mm Hg (p less than 0.05). Symptoms were alleviated and exercise capacity increased from 5.9 +/- 2.9 to 11.5 +/- 4.5 minutes (p less than 0.05). During long-term therapy, exercise capacity remained constants in three patients whereas it decreased in three others. All patients demonstrated an increase in heart size. Withdrawal of amrinone therapy precipitated severe symptoms at rest and hemodynamic deterioration in all patients. The cardiac index decreased from 1.87 +/- 0.49 to 1.32 +/- 0.30 liter/min/m2 (p less than 0.05) and pulmonary capillary wedge pressure rose from 20.6 +/- 2.9 to 28.8 +/- 5.6 mm Hg (p less than 0.05). These changes were reversed by reinstitution of therapy. Thus, amrinone-dependent hemodynamic benefits were demonstrated during long-term therapy without tachyphylaxis. In addition, progression of the underlying cardiac disease was observed in every patient.

Administration, Oral↗
PubMed1981

Medical resistance to innovation.

A certain amount of resistance to new ideas is normal and functional in science providing the innovations have a means of being tested. A number of differences between medicine and pure science are noted which can result in some medical innovations being ignored or rejected without an adequate assessment. Historical and current instances of resistance to innovation are given. Social-organizational factors in medicine appear to favor the acceptance of theoretically glamorous, pharmaceutical, and high technology innovations over simpler and less profitable ones.

Ascorbic Acid↗
PubMed1981

Coronary artery spasm and myocardial infarction in the absence of angiographically demonstrable obstructive coronary disease.

Myocardial infarction due to spasm of an "angiographically normal coronary artery" is rare, and its significance as a cause of myocardial infarction in patients without obstructive coronary disease has not been determined. Two patients are described with transmural myocardial infarction, nonobstructive coronary arteries, and suggestive evidence of coronary vasospasm as the cause of infarction. In one patient, angiography was carried out within 7 days of infarction and the documentation of normal coronary arteries argued strongly against a thromboembolic cause for infarction. This patient also had the combination of asthma, hypereosinophilia, and a systemic disease suggesting an immunologic disturbance with increased autoantibody production. A temporal association was noted between the episodes of asthma and those of coronary spasm during exacerbation of the eosinophilia, which raised the speculative issue of "allergic" coronary vasospasm. It is concluded that spasm of a nonobstructed coronary artery may cause transmural myocardial infarction. Further documentation is required in order to place this association in perspective among the other potential cause of infarction in patients with normal coronary artery anatomy.

Adult↗
PubMed1980

Comparative effects of vasodilator drugs on large and small coronary resistance vessels in the dog.

One of the mechanisms whereby nitroglycerin is considered to reduce myocardial ischaemia and spasm is its preferential reduction of resistance of large compared with small coronary arteries. Accordingly, the action of nitroglycerin on these two resistance beds was compared with newer coronary vasodilator drugs. Following intracoronary administration of boluses of each drug, large and small vessel coronary resistance was measured in 14 dogs by recording the pressure drop across each vascular bed while flow was held constant. The dose of each drug was given to reduce small vessel resistance by 30% (range means 27 to 32%) which peaked at 5 to 10 s and declined to 8 to 18% at 1 min when reduction in large vessel resistance was at its maximum. At 1 min the large vessel resistance was decreased 56 +/- 5% by nitroglycerin, 23 +/- 5% by nitroprusside, 8 +/- 4% by perhexiline, 0 +/- 5% by verapamil and increased 8 +/- 5% by nifedipine. Nitroprusside reduced the large vessel resistance significantly less than nitroglycerin (P < 0.001) for an equivalent reduction in small vessel resistance. Perhexiline, verapamil and nifedipine did not significantly reduce large vessel resistance and the discrepancy between these results and their antianginal and antispasm effect in humans was not apparent from these experiments. However, a suitable model of coronary spasm in the dog following ergonovine injection could not be created.

Animals↗
PubMed1979

Acquired pulmonary stenosis.

A patient with acquired pulmonary stenosis due to lymphocytic lymphoma is presented. Three further patients with acquired pulmonary stenosis have been seen in our department in the past 15 years. A review of published cases reveals that there are more causes of this condition than have previously been enumerated.

Adult↗