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Biomedical subjects

B H Lorell

Publications and source records attributed to B H Lorell.

At least 109 records · Page 6Linked to original sources
PubMed1985

Attenuation of coronary vascular resistance by selective alpha 1-adrenergic blockade in patients with coronary artery disease.

Alpha-adrenergic-mediated coronary vasoconstriction during stress such as cold pressor testing may contribute to myocardial ischemia by increasing coronary vascular resistance in patients with severe coronary artery disease. Nonselective alpha-receptor blockade with phentolamine abolishes both the peripheral and coronary vasoconstriction during cold pressor testing, but causes reflex tachycardia and increased inotropy. To determine the role of selective alpha 1-receptor blockade, the changes in coronary vascular resistance during cold pressor testing were measured in 18 patients with coronary artery disease before and after intravenous administration of 100 mg of trimazosin. Cold pressor testing was performed at a constant paced subanginal heart rate of 95 +/- 5 beats/min (+/- 1 SD). Before trimazosin, cold pressor testing increased mean arterial pressure by 9 +/- 4% (102 +/- 14 to 111 +/- 14 mm Hg, p less than 0.001) with no change in coronary sinus blood flow, but significantly increased coronary vascular resistance by 15 +/- 19% (1.02 +/- 0.46 to 1.15 +/- 0.57 units, p less than 0.05). Five minutes after trimazosin, cold pressor testing increased mean arterial pressure by 6 +/- 5% (p less than 0.001) with a marked attenuation of the increase in coronary vascular resistance (6 +/- 11%, p = NS), which was significantly less than before trimazosin (p less than 0.02). Trimazosin did not increase plasma norepinephrine concentration at rest, suggesting that in the dosage used trimazosin caused selective alpha 1-receptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1984

Effects of verapamil on contraction and relaxation of cultured chick embryo ventricular cells during calcium overload.

The calcium channel blocking agents verapamil and nifedipine have been reported to lessen abnormalities of left ventricular relaxation in patients with severe left ventricular hypertrophy or coronary artery disease. Whether these effects in human beings are related in part to a direct effect on myocardial calcium metabolism is difficult to determine because of complicating drug influences on ventricular loading via systemic arterial vasodilation, on myocardial blood supply via coronary artery vasodilation and on reflex changes in sympathetic tone. For this reason, the effects of verapamil were investigated in a cellular model of impaired relaxation using spontaneously contracting tissue cultured monolayers of chick embryo ventricular cells exposed to high external calcium ([Ca]o). Under control conditions ([Ca]o, 0.9 mM), verapamil (2 X 10(-8)M) induced a 57 +/- 8% decrease in amplitude of cell contraction monitored with a phase contrast microscope video motion detector system. Elevation of [Ca]o from 0.9 to 8.0 mM resulted in a decrease in amplitude and velocity of contraction and a decrease in velocity of relaxation associated with an upward shift in diastolic cell wall position, suggesting a failure of normal myofilament dissociation. These abnormalities were completely reversible on reperfusion with [Ca]o, 0.9 mM. On re-exposure of the cells to [Ca]o, 8.0 mM, in the presence of verapamil, there was an increase in amplitude of contraction (0.56 +/- 0.11 to 1.03 +/- 0.09 micron, p less than 0.01) and velocity of relaxation (4.97 +/- 0.89 to 9.94 +/- 0.87 micron/s, p less than 0.01) compared with exposure to [Ca]o, 8.0 mM, alone, and an attenuation of the upward shift in diastolic cell wall position.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Phaeochromocytoma and hypertrophic cardiomyopathy: apparent suppression of symptoms and noradrenaline secretion by calcium-channel blockade.

A 44-year-old woman with hypertrophic cardiomyopathy and a noradrenaline-secreting phaeochromocytoma is described. She experienced as great improvement in cardiovascular symptoms during double-blind treatment with the calcium-channel blocker nifedipine compared with the placebo period. Symptom relief on nifedipine therapy was associated with a pronounced decline in elevated urinary noradrenaline levels. This observation suggests that calcium-channel blockers interfere with the release of noradrenaline from phaeochromocytoma tissue and thus may be beneficial in patients with phaeochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1983

Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation?

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.

Adolescent↗
PubMed1983

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

The left ventricular diastolic pressure-volume relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and M-mode echocardiography before and during angina induced by pacing tachycardia. All patients had two- or three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development of angina and a postpacing rise in left ventricular end-diastolic pressure (15 +/- 3 to 31 +/- 6 mm Hg, p less than 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 +/- 2.1 to 9.2 +/- 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 +/- 37 to 48 +/- 27 mm/sec, p less than 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 +/- 5 to 58 +/- 7 msec, p less than 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (sigma R = -PR). A radial stiffness modulus (ER) was determined by the slope of the PR vs log h plots before and after pacing. Over the same range of residual radial stress (sigma R), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.

Adult↗
PubMed1983

Potentiation of coronary vasoconstriction by beta-adrenergic blockade in patients with coronary artery disease.

Although beta-adrenergic blocking agents reduce myocardial oxygen consumption and symptoms of myocardial ischemia in patients with coronary artery disease (CAD), propranolol has been reported to exacerbate coronary artery spasm in some patients with variant angina. To determine whether increased coronary vasomotor tone can be induced by beta-adrenergic blockade, we measured the changes in coronary vascular resistance (CVR) during cold pressor testing (CPT) in 15 patients, nine with severe CAD and six with normal left coronary anatomy, before and after i.v. propranolol (0.1 mg/kg). Coronary blood flow was measured by coronary sinus thermodilution. CVR was calculated as mean arterial pressure divided by coronary sinus blood flow. Heart rate was maintained constant at a paced subanginal rate of 95 +/- 5 beats/min. Before propranolol, CPT induced significant increases in coronary vascular resistance in patients with CAD (15.0 +/- 2.2%, p less than 0.02), but no increase in CVR in the normal patients. After propranolol, the CVR change during CPT was augmented for patients with CAD (29 +/- 6%, p less than 0.01) and for the normal population (9 +/- 5%, NS). The potentiated increase in CVR occurred without significant changes in resting CVR or in the magnitude of the hypertensive response to CPT. We conclude that beta-adrenergic blockade with propranolol can potentiate coronary artery vasoconstriction in some patients with CAD, possibly mediated by unopposed alpha-adrenergic vasomotor tone. These changes may be important in patients in whom intense adrenergic stimulation may increase coronary artery tone and adversely influence the balance between myocardial oxygen supply and demand.

Adrenergic beta-Antagonists↗
PubMed1983

Potentiation of the cardiovascular effects of nitroglycerin by N-acetylcysteine.

The biochemical basis of the mechanism of vasodilatation by nitroglycerin (NTG) has not been previously investigated in man. However, evidence from in vitro studies suggests that NTG induces activation of guanylate cyclase via a series of enzymatic reactions that are modulated by the availability of sulfhydryl groups. Cysteine appears to be particularly effective in potentiating guanylate cyclase activation by NTG. To determine whether hemodynamic responsiveness to NTG in man might be modulated by sulfhydryl availability, concentration-response curves for effects of intravenously infused NTG on mean arterial pressure (MAP) and mean pulmonary capillary wedge pressure (PCW) were obtained in 10 patients undergoing cardiac catheterization for investigation of chest pain. NTG infusion was repeated 10 min after the intravenous infusion of 100 mg/kg of the cysteine source N-acetylcysteine (NAC). NAC induced no significant hemodynamic effect, but after NAC infusion there was a significant reduction both in the NTG infusion rate associated with a 10% fall from control values in MAP (25.8 +/- 8.3 to 9.3 +/- 2.7 micrograms/min; p less than .01) and in the infusion rate inducing a 30% reduction in PCW (13.6 +/- 4.6 to 4.2 +/- 1.6 micrograms/min; p less than .02). In a control group of five patients who received no NAC, there was no significant change in responsiveness to NTG between infusions. It is concluded that NAC potentiates the vasodilator effects of NTG in man. This suggests that sulfhydryl availability and/or redox state may be determinants of in vivo responsiveness to NTG.

Acetylcysteine↗
PubMed1983

Recognition and management of pulmonary hypertension.

Pulmonary hypertension is a common manifestation of many diverse diseases. In most cases, the cause of elevated pulmonary arterial pressure is apparent on the basis of history, physical examination, chest x-ray, and ancillary noninvasive tests such as blood gases, pulmonary function tests, or echocardiography. Occasionally, more invasive tests such as cardiac catheterization and pulmonary angiography may be necessary. In those patients in whom no cause can be found, the pulmonary hypertension is labeled as primary or idiopathic. Effective therapy exists for alleviating pulmonary hypertension in most cases of secondary pulmonary hypertension. The prognosis of patients with primary pulmonary hypertension is dismal, although encouraging reports are beginning to appear regarding the use of vasodilators.

Adult↗
PubMed1982

Modification of abnormal left ventricular diastolic properties by nifedipine in patients with hypertrophic cardiomyopathy.

The effect of nifedipine on left ventricular isovolumic relaxation and diastolic filling properties and systemic and left ventricular hemodynamics was studied in 15 patients with hypertrophic cardiomyopathy. After nidefipine (10 mg sublingually), the prolonged left ventricular isovolumic relaxation time assessed by echocardiography decreased from 112 +/- 26 to 83 +/- 23 msec (p less than 0.0001), and the left ventricular pressure decay as measured by time constant T improved from 63 +/- 20 to 49 +/- 11 msec (p less than 0.05). Left ventricular filling dynamics also improved as assessed by a return toward normal in the depressed peak rate of left ventricular diastolic filling (dimension change 72 +/- 37 to 101 +/- 39 mm/sec, p less than 0.01) and the peak rate of posterior wall thinning (47 +/- 31 to 68 +/- 36 mm/sec, p less than 0.001). These changes were accompanied by hemodynamic evidence of improved diastolic function shown as a decrease in left ventricular end-diastolic pressure and a downward shift in the left ventricular diastolic pressure-dimension relationship, suggesting improved left ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic arterial blood pressure, and no depression of the left ventricular percent fractional shortening or cardiac index. These data indicate that abnormal left ventricular relaxation and diastolic filling rates in hypertrophic cardiomyopathy are dynamic and favorably modified by nifedipine, and that this effect is not related to a depression of left ventricular systolic function.

Adolescent↗
PubMed1982

Beneficial effects of nifedipine on regional myocardial blood flow in patients with coronary artery disease.

Nifedipine inhibits the slow-channel calcium current, which plays a major role in vascular smooth-muscle contraction. However, the effect of nifedipine on regional myocardial blood flow (RMBF) in patients with coronary artery disease (CAD) is unknown. In 18 patients with chest pain syndromes, RMBF was determined with xenon-133 before and after nifedipine. In patients with CAD. 25 regions were analyzed distal to significant coronary obstruction(greater than 70% reduction in luminal diameter) and eight regions were analyzed in patients with normal coronary arteries. In patients with CAD, RMBF increased in 21 of 25 regions (average 17.4 /+- 5.7%,p less than 0.01), but decreased in all eight regions in patients with normal coronary arteries, by an average of 14.4 /+- 2.3% (p less than 0.01). The difference between groups was significant (p less than 0.01). In our patients with CAD, improved RMBF appears to be related to a decrease in coronary vascular tone and suggests a physiologic basis for the beneficial effect of nifedipine in ischemic heart disease.

Adult↗
PubMed1981

Modification of left ventricular response to pacing tachycardia in nifedipine in patients with coronary artery disease.

The calcium blocking agent nifedipine was shown to protect the isolated left ventricle against the development of altered diastolic compliance during severe global ischemia. To assess the influence of nifedipine during myocardial ischemia in human subjects, we studied the effect of nifedipine (20 mg sublingually) on the hemodynamic response to pacing tachycardia (heart rate 66 +/- 4 to 143 +/- 4 beats per minute) in 17 patients with multivessel coronary artery disease. Typical anginal pain occurred in all patients during pacing tachycardia before nifedipine, but in only 3 of 17 patients during pacing after nifedipine. In 11 patients a significant (greater than or equal to 5 mm Hg) increase in postpacing left ventricular end-diastolic pressure (LVEDP, 15 +/- 2 mm Hg to 28 +/- 2 mm Hg, p less than 0.01) developed, and was associated with an upward shift of the left ventricular diastolic pressure-volume curve. In these patients, pretreatment with nifedipine did not alter resting LVEDP or aortic pressure, but did attenuate or abolish the increase n LVEDP and the shift in left ventricular diastolic pressure-volume curves after pacing tachycardia to the same rate and for the same duration. The antianginal effect of nifedipine was not associated with a reduction in contractility, because there was no change in LV + dp/dt after nifedipine. However, the increase in left ventricular systolic pressure achieved in response to pacing tachycardia was less after nifedipine. We conclude that nifedipine favorably modifies the symptomatic and hemodynamic response to pacing tachycardia in patients with coronary artery disease. The mechanism is uncertain and could involve a direct myocardial effect, peripheral vasodilation, coronary vasodilation or a combination of these effects.

Calcium Channel Blockers↗
PubMed1981

Right ventricular distension and left ventricular compliance.

The constraint of the right ventricle (RV) on the end-diastolic pressure-volume (PV) relationship of the nonischemic and ischemic left ventricle (LV) was studied. The model used was the isovolumic beating LV, with separately perfused ejecting RV with controlled RV distension. The effect of augmented RV distension on the nonischemic LV PV relationship was examined. A change from mild [right ventricular end-diastolic pressure (RVEDP) = 1.5 mm Hg] to severe (RVEDP = 16 mmHg) RV distension resulted in a significant leftward shift of the LV PV relationship. Ischemia was produced for 90 min by reducing flow in the cannulated left main coronary artery and the effect of two levels of stable RV distension on the PV relationship of the ischemic LV was examined. Mild RV distension and moderate (RVEDP = 6 mmHg) RV distension were used. In both groups, there was a progressive leftward shift in the LV PV relationship that was significant by 60 min of ischemia. No change was seen in nonischemic controls. Ventricular relaxation, as described by the time constant of isovolumic relaxation, T, was impaired throughout ischemia but was not sufficiently prolonged to explain the above changes. Thus, the time course of change in the LV PV relationship during ischemia differs from that previously reported after pacing-induced ischemia in humans. Neither the external constraint of the RV nor incomplete relaxation explains this difference.

Animals↗
PubMed1981

Acute effects of oral pirbuterol on myocardial oxygen metabolism and systemic hemodynamics in chronic congestive heart failure.

Pirbuterol hydrochloride, an orally effective beta-adrenergic agonist, improves hemodynamic abnormalities in patients with congestive heart failure, but its effects on myocardial oxygen consumption (MVO2) and coronary blood flow have not been characterized. We studied the effects of 20-30 mg of oral pirbuterol on myocardial metabolic and hemodynamic parameters in 12 patients (six with coronary artery disease) with chronic CHF refractory to standard medical therapy. Pirbuterol induced an increase in cardiac index (1.7 +/- 0.1 to 2.3 +/- 0.2 l/min/m2, p less than 0.05) and a fall in systemic vascular resistance (1884 +/- 118 to 1391 +/- 69 dyn-sec-cm-5, p less than 0.01) 2 hours after administration. Pulmonary capillary wedge pressure fell from arterial and right atrial pressures did not change. Heart rate remained constant. Arterial-coronary sinus oxygen content difference narrowed (from 12.9 +/- 0.4 to 11.1 +/- 0.3 vol%, p less than 0.05), while no significant change occurred in MVO2. Myocardial oxygen extraction ratio and myocardial lactate extraction ratio did not change, and no patient developed angina or electrocardiographic evidence of myocardial ischemia. Patients with coronary artery disease had hemodynamic and myocardial metabolic responses similar to those without coronary artery disease. Pirbuterol effects substantial acute hemodynamic improvement in patients with chronic congestive heart failure without increasing requirements for coronary blood flow or myocardial oxygen delivery and without provoking myocardial ischemia.

Adult↗
PubMed1981

Constrictive pericarditis: a case requiring pericardiectomy following Dressler's postmyocardial infarction syndrome.

Exertional neck tightness developed 6 months following a myocardial infarction that was complicated by Dressler's syndrome. The patient's symptoms were initially interpreted as angina pectoris but did not respond to antianginal therapy. Findings at cardiac catheterization were indicative of constructive pericarditis. The diagnosis was confirmed at pericardiectomy and the symptoms resolved completely postoperatively. Constrictive pericarditis should be considered as an unusual but important sequel of Dressler's postmyocardial infarction syndrome.

Cardiac Catheterization↗
PubMed1980

Pulmonary hypertension in systemic lupus erythematosus: hemodynamics and effects of vasodilator therapy.

A case is reported of a 29-year-old woman with systemic lupus erythematosus (SLE) who developed clinical manifestations of pulmonary hypertension at a time when other manifestations of SLE were quiescent. She had a restrictive ventilatory defect but clear lung fields on chest x ray. Cardiac catheterization revealed severe pulmonary hypertension. Calculated pulmonary vascular resistance fell slightly after administration of oxygen and during infusion of vasodilators. Symptomatic improvement and a modest increase in right ventricular ejection fraction, as measured by radionuclide ventriculography, were noted following 1 week of oral hydralazine therapy. Clinically significant pulmonary hypertension is a rare complication of SLE and the increased pulmonary vascular resistance may not be entirely fixed. Cardiac catheterization and radionuclide ventriculography may be useful in assessing response to medical therapy.

Adult↗