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Biomedical subjects

J L Halperin

Publications and source records attributed to J L Halperin.

At least 55 records · Page 3Linked to original sources
PubMed1989

Angiosarcoma of the left atrium mimicking myxoma: case report.

The case of a 65-year-old female patient with a pedunculated left atrial angiosarcoma is presented. Histologically, the tumor was composed of vascular spaces lined by atypical cells with similar cells in the solid portion of the tumor. Immunohistochemical stain for factor VIII-related antigen was positive in the cells forming vascular spaces. Immunoperoxidase stain for Ulex Europaeus I lectin was positive in cells lining vascular lumina and in individual cells in the solid portion of the tumor. Cardiac angiosarcomas characteristically occur in men, arise in the right atrium, are large mural masses that infiltrate widely at the time of presentation, and are usually rapidly fatal. Review of the literature reveals that this case of cardiac angiosarcoma is unusual by virtue of its occurrence in a female, left atrial location as a polypoid lesion, and prolonged symptom-free survival after surgical resection alone. Cardiac angiosarcoma may clinically and radiologically simulate myxoma.

Aged↗
PubMed1988

The prevalence and one-year outcome of limb arterial obstructive disease in a nursing home population.

To assess the utility of bedside diagnostic measures to detect prognostically significant peripheral vascular disease, we examined 60 nursing home residents by physical examination, Doppler sphygmomamometry and pneumatic oscillometry, and recorded the clinical history. Eighty-eight percent of the cases had tibial/brachial arterial systolic pressure indices below 0.95, the lower limit traditionally considered normal. Yet, no more than 5% of the patients carried a previous diagnosis of peripheral vascular disease or had intermittent claudication, leg ulcers or gangrene. Approximately half of the patients had tibial/brachial pressure indices less than 0.7, and one year later in these cases, there was significantly greater morbidity and nearly twice the mortality of patients with less severe disease. We conclude that simple bedside diagnostic tests of arterial disease used in this study discloses a high prevalence of disease in institutionalized elderly patients and identifies a group at particular risk for morbid complications.

Aged↗
PubMed1987

Effect of nitroglycerin during hemodynamic estimation of valve orifice in patients with mitral stenosis.

In patients with mitral stenosis, valve orifice calculations using pulmonary capillary wedge pressure as a substitute for left atrial pressure may overestimate the severity of disease. Previous studies have shown that mitral valve area determined from transseptal left atrial pressure measurements exceeds that area derived from pulmonary wedge pressure measurements. This is probably due to pulmonary venoconstriction, which is reversed by nitroglycerin. Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable. At the time of a peak hypotensive effect, 3 to 5 minutes after nitroglycerin administration, the mean pulmonary capillary wedge pressure decreased from 23 +/- 2 (mean +/- SEM) to 19 +/- 2 mm Hg (p less than 0.005). The mean diastolic transmitral pressure gradient (12.6 +/- 1.2 mm Hg before and 11.5 +/- 1.0 mm Hg after nitroglycerin; p = NS) and cardiac output (4.0 +/- 0.3 to 4.1 +/- 0.3 liters/min; p = NS) did not change significantly. Nevertheless, the hemodynamic mitral orifice area, calculated using the Gorlin formula, increased from 0.8 +/- 0.1 to 1.1 +/- 0.2 cm2 (p less than 0.05). In 12 patients with isolated mitral stenosis, without regurgitation, the mitral valve orifice area after nitroglycerin was 0.4 +/- 0.2 cm2 larger than it was before drug administration (p less than 0.05). Administration of nitroglycerin during evaluation of mitral stenosis eliminates pulmonary venoconstriction, which raises the pulmonary capillary wedge pressure above the left atrial pressure in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Extraluminal compression of an aortic graft simulating recoarctation.

Restenosis rarely develops after surgical correction of coarctation of the aorta in adults. Late morbidity is usually related to residual hypertension or progressive aortic valve disease. A patient in whom symptoms and signs of recurrent coarctation developed 19 years after initial graft repair is described. Dehiscence of the original silk suture line was found at operation. Extensive thrombus had produced graft compression. Milder hypertension persisted in the postoperative period despite relief of the aortic obstruction.

Adult↗
PubMed1987

Peripheral vascular disease: medical evaluation and treatment.

Peripheral arterial obstructive disease with symptoms of ischemia in the limbs is a common cause of disability, morbidity, and even mortality in the elderly. The most important cause is atherosclerosis, which is ultimately a systemic problem, but the cardinal symptom in the limbs is intermittent claudication. Unfortunately, the elderly patient often displays severe ischemia with pain at rest, and ulceration or gangrene of the extremity, even where there was a paucity of prior claudication, perhaps due to associated illness which reduces mobility. The essential aspects of clinical diagnosis and assessment of severity of ischemia involve relatively simple bedside techniques, and noninvasive laboratory methodology is mainly of value in selection of patients for angiography and potential revascularization. While conventional therapy involves bypass surgery, an expanding array of drugs and the advent of interventional angiographic measures including angioplasty offer alternatives which were not available even a few years ago.

Aged↗
PubMed1986

Effect of labetalol on limb haemodynamics in patients following coronary artery bypass graft surgery.

Labetalol is a competitive inhibitor of alpha- and beta-adrenergic receptors and has an antihypertensive action. To determine limb haemodynamic effects, we measured calf blood flow and venous capacitance by venous occlusion plethysmography before and after oral labetalol in 10 patients 3-7 days following coronary bypass surgery. Vascular resistance was calculated as the ratio of mean arterial pressure to arterial flow. The peak effect of labetalol was taken as the point of maximum blood pressure decline, and this interval was selected for evaluation of the limb haemodynamic response. Ninety to 120 min after administration of 100-200 mg of labetalol the mean blood pressure fell from 88 +/- 3 to 79 +/- 3 mm Hg; (P less than 0.005). The mean arterial blood flow registered 5.1 +/- 1.0 ml 100 ml-1 limb tissue min-1 which was not significantly different from the control value of 4.4 +/- 0.8 ml 100 ml-1 limb tissue min-1. The calculated index of limb vascular resistance was not affected by labetalol administration, averaging 37 +/- 12 mm Hg 100-1 ml limb tissue min-1 before labetalol and 30 +/- 11 mm Hg ml-1 100 ml limb tissue min-1 at the time of peak hypotensive effect. There was a slight but statistically significant increment in limb venous volume to 1.9 +/- 0.3 from 1.5 +/- 0.3 ml 100 ml-1 limb tissue (P less than 0.025). Placebo administration produced no consistent changes in blood pressure, arterial blood flow, vascular resistance or venous capacitance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1985

Femoral pseudoaneurysm following nonpenetrating trauma in a patient with aortic insufficiency.

Although not uncommon after penetrating vascular trauma, arterial pseudoaneurysms rarely develop following blunt trauma. A patient is described in whom indirect trauma led to pseudoaneurysm of the profunda femoris artery, and persistent bleeding required surgical intervention. In this case, the coexistence of significant aortic valvular regurgitation suggests that wide pulse pressure may predispose to this arterial complication.

Aged↗
PubMed1985

Effect of nitroglycerin on the pulmonary venous gradient in patients after mitral valve replacement.

Because the equality of the pulmonary artery wedge pressure and left atrial pressure has been questioned in patients with mitral valve disease and pulmonary hypertension, this study examined how vasomotor activity in the pulmonary capacitance vessels might contribute to a discrepancy between these pressures. The difference between the pulmonary wedge and left atrial pressures (designated as the pulmonary venous gradient) was measured after nitroglycerin administration in nine patients who had pulmonary hypertension (mean pulmonary artery pressure 40 mm Hg) after mitral valve replacement. Five minutes after sublingual nitroglycerin, 0.4 mg, the mean pulmonary wedge pressure decreased from 19 +/- 2 to 13 +/- 2 mm Hg (p less than 0.005), exceeding the decrease in left atrial pressure (15 +/- 2 to 11 +/- 2 mm Hg; p less than 0.005). Pulmonary blood flow increased from 4.6 +/- 0.4 to 4.9 +/- 0.4 liters/min (p less than 0.005). The decrease in mean pulmonary venous gradient from 4.0 +/- 0.8 to 1.7 +/- 0.6 mm Hg (p less than 0.025) was attributed to nitrate-mediated pulmonary venodilation. The ratio of venous gradient to blood flow, an index of pulmonary venous tone, decreased after nitroglycerin from 0.9 +/- 0.2 to 0.4 +/- 0.1 (p less than 0.01). These data indicate that reversible pulmonary vasoconstriction contributes to elevation of the pulmonary wedge pressure above the left atrial pressure in patients with chronic mitral valve disease and pulmonary hypertension and that nitroglycerin may produce pulmonary venodilation decreasing the pulmonary venous gradient.

Adult↗
PubMed1985

Unilateral neck pulsations in a patient with a permanent pacemaker.

An asymptomatic patient with a permanent pacemaker presented with unilateral accentuated neck pulsations. Evaluation revealed tricuspid insufficiency, a massively dilated right internal jugular vein, and obstruction of the left internal jugular vein. There was no evidence of aneurysm, vascular tumor, or fistula. The most likely explanation for this constellation of findings is tricuspid regurgitation occurring in the setting of unilateral internal jugular vein occlusion. Such a combination should be considered in the differential diagnosis of asymmetrical neck pulsations in a patient with a transvenous pacemaker.

Humans↗
PubMed1984

Myopotential interference with DDD pacemakers: endocardial electrographic telemetry in the diagnosis of pacemaker-related arrhythmias.

Skeletal myopotentials may inhibit the output of unipolar demand ventricular pacemakers, resulting in protracted episodes of asystole in susceptible patients. The new DDD-mode pacemakers have, in addition to a unipolar ventricular lead, a unipolar atrial lead to enable atrioventricular sequential or atrial synchronous function. During clinical investigation of a new dual-unipolar cardiac pacing system programmed to operate in the DDD mode (Pacesetter AFP models 281 and 283), 6 patients were noted (5 men and 1 woman, aged 22 to 68 years) who manifested paroxysmal acceleration of ventricular pacing rate approaching the maximal tracking rate. Two patients also had abrupt slowing or cessation of ventricular output. With the use of atrial electrographic recordings (obtained with telemetry), the following mechanisms of rate change were found: myopotential tracking, myopotential inhibition, interference-mode asynchronous operation, sudden increases in sinus rate, and pacemaker-mediated reentrant tachycardia. In all patients, reprogramming of the implanted devices, based on telemetered atrial electrography, resulted in disappearance of the arrhythmias and loss of symptoms while maintaining the DDD pacing mode. Thus, several mechanisms of rhythm disturbances are peculiar to dual-chamber cardiac pacing systems that use unipolar electrodes. Endocardial telemetry combined with extensive programming capability offers the best opportunity for proper diagnosis and management of these problems.

Adult↗
PubMed1984

Nitroglycerin therapy in the management of pulmonary hypertensive disorders.

Vasodilator therapy has not been effective in patients with pulmonary hypertension because most of the drugs that have been utilized in treating this disorder do not exert selective effects on the pulmonary circulation. Nonselective agents may cause predominant systemic vasodilation and lead to severe hypotension; they may elicit reflex activation of the sympathetic nervous system and further elevate pulmonary artery pressures; or they may exert depressant effects on right ventricular function and aggravate right-sided heart failure. Nitroglycerin has theoretic appeal as a vasodilator drug in patients with pulmonary hypertension because it exerts a direct effect on the pulmonary circulation in doses that do not affect systemic resistance vessels or the myocardium and do not activate neurohumoral reflexes. Furthermore, the drug uniquely reduces pulmonary artery pressures in addition to pulmonary vascular resistance due to its ability to dilate venous capacitance vessels. Preliminary studies with sublingual and intravenous nitroglycerin in patients with pulmonary hypertension have shown that the drug produces marked hemodynamic improvement and that clinical benefits follow long-term therapy with transcutaneous or oral nitrates. However, treatment may provoke hypotensive events in some patients and systemic hypoxemia in others; still others may fail to benefit because the pulmonary vasculature is unresponsive to any vasodilator stimulus. Further work is needed to define the benefits and risks of nitroglycerin therapy in patients with pulmonary hypertension.

Humans↗
PubMed1984

Redistribution of regional blood flow following angiotensin-converting enzyme inhibition. Comparison of normal subjects and patients with heart failure.

The systemic and regional circulatory effects of angiotensin-converting enzyme inhibition were investigated in 30 normal subjects and in 36 patients with severe congestive heart failure. Regional blood flow was measured in individual patient groups. Cardiac index rose and systemic vascular resistance fell in normal subjects after angiotensin-converting enzyme inhibition. In the patients with heart failure, a similar rise in cardiac index and fall in systemic resistance occurred. In addition, right and left ventricular filling pressures decreased. The fall in systemic vascular resistance correlated with plasma renin activity (r = 0.57, p less than or equal to 0.001). Of the regional circulations investigated in normal subjects, only forearm blood flow increased after angiotensin-converting enzyme inhibition. Although over-all there was no change in renal or coronary blood flow, coronary flow dramatically increased in some patients and the increase in flow correlated with plasma renin activity (r = 0.939, p less than or equal to 0.001). In patients with heart failure, forearm, splanchnic, and coronary flow were unaffected by angiotensin-converting enzyme inhibition, whereas renal blood flow estimated from para-aminohippurate clearance increased 60 percent and accounted for 50 percent of the increase in cardiac output seen in these patients. Thus, redistribution of flow occurs in congestive heart failure with a significant reduction in the fraction flow to the kidneys when compared with normal flow. The contribution of the renin-angiotensin system to the regulation of regional blood flow is different in normal subjects and in patients with heart failure. Angiotensin-converting enzyme inhibition augments skeletal flow in normal subjects whereas it increases renal blood flow in patients with heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

Digital vasodilatation during mental stress in patients with Raynaud's disease.

Fingertip blood flow was measured by venous occlusion plethysmography before and during a stressful mental task consisting of rapid serial arithmetic calculations in a 25 degrees C room. Significant rises in heart rate and blood pressure indicated that stress was actually induced in all individuals. During mental stress in normal subjects, blood flow decreased (46.4 +/- 6.2 to 22.4 +/- 4.9 ml X min-1 per 100 ml tissue; P less than 0.01) and vascular resistance increased (2.1 +/- 0.4 to 7.6 +/- 2.2 units; P less than 0.01). Patients with Raynaud's disease unexpectedly increased blood flow (15.4 +/- 4.2 to 21.6 +/- 5.7; P = 0.05) and decreased vascular resistance (9.7 +/- 2.3 to 7.1 +/- 1.4; P = 0.05). Ten additional normal subjects were studied in a cool room (20 degrees C). Their digits remained vasoconstricted during stress, as blood flow (7.4 +/- 2.9 to 5.1 +/- 1.3) and vascular resistance (31.5 +/- 11.1 to 34.4 +/- 8.2) varied insignificantly (P greater than 0.10). The digital vasodilatation which occurs during mental stress in patients with Raynaud's disease was not altered by pretreatment with oral indomethacin, with intra-arterial propranolol or atropine, or by digital nerve block. These findings suggest the existence of an active digital vasodilatory mechanism in patients with Raynaud's disease.

Adult↗