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Biomedical subjects

B Lorell

Publications and source records attributed to B Lorell.

7 recordsLinked to original sources
PubMed1988

Doppler evidence that true left ventricular-to-aortic pressure gradients exist in hypertrophic cardiomyopathy.

The etiology of systolic left ventricular-to-aortic pressure gradients in hypertrophic cardiomyopathy is still controversial. While cavity obliteration has been proposed by some investigators as the cause for recording of a high left ventricular systolic pressure, the concept of left ventricular outflow tract obstruction has received more experimental support. To investigate further whether left ventricular pressure truly exceeds aortic pressure and implies obstruction, we studied, with imaging and Doppler echocardiographic techniques, five patients with asymmetric septal hypertrophy and systolic anterior movement of the mitral valve occasionally causing it to abut upon the septum. All had outflow tract pressure gradients (peak 85 +/- 10 mm Hg) and trace to mild mitral regurgitation. Continuous wave Doppler study recorded peak flow velocities in the outflow tract (4.6 +/- 0.3 m/sec), and mitral regurgitant (mean 6.6 +/- 0.3 m/sec) jets. Aortic systolic and diastolic blood pressures were measured by cuff sphygmomanometry, and simultaneous carotid pulse tracings were recorded. The magnitude of systolic aortic pressure was determined at the time of peak velocity in the mitral regurgitant jet. Since the peak systolic pressure gradient across the mitral valve (left ventricular minus left atrial pressure) should equal 4 times the square of the peak velocity (V) in the mitral regurgitant jet, peak left ventricular systolic pressure should equal 4 x V2 plus the height of left atrial pressure at the time of peak mitral regurgitant velocity. In each case, calculations were made assuming an upper normal left atrial pressure of 10 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomyopathy, Hypertrophic↗
PubMed1982

Hypoxia, calcium fluxes, and inotropic state: studies in cultured heart cells.

Methods have been developed for the study of cellular mechanisms underlying a variety of physiologic and pathophysiologic phenomena using cultured chick embryo heart cells. These spontaneously beating monolayer preparations lack appreciable diffusion barriers, and interstitial space components can be defined and controlled conveniently. These properties facilitate the measurement of transmembrane fluxes and cellular contents of sodium, potassium, and calcium. Concomitantly, methods have been developed to measure the contractile state as reflected in the amplitude and velocity of movement of individual myocytes in the culture. Experiments are described in which the contractile responses of cultured heart cells to graded hypoxia demonstrated a critical PO2 level around 12 mm Hg, below which progressive impairment of contractile function occurred. In preparations with iodoacetate-induced glycolytic blockade, enhanced sensitivity to hypoxia occurred. Although experiments are described, demonstrating the applicability of this model system to the study of problems including the mechanism of cardiac glycoside-induced increases in inotropic state and the definition of calcium flux pathways important in excitation-contraction coupling.

Animals↗
PubMed1980

Regional differences in pulmonary vascular resistance in the same patient. A study of partial anomalous pulmonary venous return, intact atrial septum, and mitral stenosis before and after surgical correction.

Using hemodynamic and radionuclide perfusion data, we measured regional pulmonary vascular resistances in a patient with mitral stenosis and anomalous pulmonary venous drainage with intact atrial septum before and after surgical correction. Pulmonary vascular resistance in the right upper lung region that had anomalous drainage to a normal-pressure right atrium was compared to resistance of a region in the left upper lung similar in size that had normal drainage to a high-pressure left atrium. Preoperatively, pulmonary vascular resistance in both regions was elevated but was considerably higher in the left upper lung region. Postoperatively, pulmonary vascular resistance fell substantially in the left upper lung with the fall in left atrial pressure, whereas it changed minimally in the right upper lung after elimination of the left-to right shunt. These findings are related to vascular abnormalities on biopsies obtained from both regions.

Female↗
PubMed1979

Right ventricular infarction. Clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction.

Twelve patients with a clinical diagnosis of right ventricular infarction are described. All had acute inferior wall myocardial infarction associated with the bedside findings of jugular venous distension, clear lungs on auscultation, and arterial hypotension. Hemodynamically, there was elevation of right-sided filling pressures not explained by normal or minimally elevated pulmonary wedge pressures. Four patients had an incorrect diagnosis of acute cardiac tamponade. However, a review of the data showed that the hemodynamic features of right ventricular infarction more closely resemble those of pericardial constriction, a point that may be helpful in distinguishing right ventricular infarction from cardiac tamponade. Invasive and noninvasive techniques that exclude the presence of pericardial fluid and suggest enlargement and abnormal contractility of the right ventricle were helpful in establishing the diagnosis of right ventricular infarction in several patients.

Aged↗
PubMed1979

Atrial flutter with exit block.

The mechanism of atrial flutter is controversial. A 76-year-old woman with rheumatic heart disease was referred to our clinic with an unusual rhythm disturbance which initially appeared to be classic atrial flutter at a rate of 300 beats/min. Later tracings, however, demonstrated a rate exactly one-half that of the earlier ECGs, with an identical p-wave morphology and vector. This latter rhythm also behaved in a manner expected for a flutter mechanism in that both spontaneously and with carotid pressure high-degree atrioventricular block occurred without alteration of the underlying atrial mechanism. Finally, the two rates interchanged spontaneously over several days without any significant interval changes in medical therapy. These findings were initially explained as probable digoxin toxicity. The underlying mechanism, however, was more likely atrial flutter with exit block and in this patient may have represented another facet of her sick sinus syndrome. This unusual phenomenon is discussed in terms of previous reports and possible implications for the mechanism of atrial flutter.

Aged↗
PubMed1978

Cardiac sarcoidosis. Diagnosis with endomyocardial biopsy and treatment with corticosteroids.

A 27 year old woman was hospitalized for progressive dyspnea, fatigue and retrosternal chest pain. She had progressive cardiac enlargement with clinical and laboratory confirmation of a dilated cardiomyopathy. Transvenous percutaneous right ventricular endomyocardial biopsy yielded a specimen showing a noncaseating granuloma. The patient's dyspnea responded dramatically to steroid therapy with corresponding improvement in radiographic and echographic measures of ventricular performance. This case illustrates the problem of diagnosing cardiac sarcoidosis when there is no apparent evidence of other organ involvement.

Adult↗