Biomedical subjects
J J Leonard
Publications and source records attributed to J J Leonard.
Clinical competence in exercise testing. A statement for physicians from the ACP/ACC/AHA Task Force on Clinical Privileges in Cardiology.
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Usefulness of Doppler echocardiography in the management of patients with mitral stenosis during pregnancy.
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Adult cardiology and the expanding supply of physicians.
The number of cardiologists can be projected with considerable accuracy into the next century. The total cardiology pool of physicians will increase until the year 2015 at which time those entering and leaving the pool will come into equilibrium. At that time the ratio of active cardiologists to the population will have greatly increased. This nation's future need for cardiologists is difficult to assess with any degree of precision. Therefore, this is the time for updating practice profile studies. Such studies today could be formulated in a manner to provide more detailed information on the cardiologist's daily activities. In addition, a data base developed through methodology such as the consensus formation approach must be developed and updated on a periodic basis. Through such analyses it will be possible to quantitate the future needs of cardiovascular manpower.
Prevalence of systolic anterior motion of the mural (posterior) leaflet of the mitral valve in hypertrophic cardiomyopathy: an echocardiographic study.
Cross-sectional echocardiography was used to identify systolic anterior motion of the mural (posterior) leaflet of the mitral valve from a group of 53 patients with hypertrophic cardiomyopathy. This type of systolic anterior motion was identified in parasternal long axis, apical four-chamber and/or long-axis cross-sections and was characterized by an elongation of the mural leaflet and an abnormal coaptation with the aortic (anterior) leaflet. At end-diastole, the aortic leaflet coapted at the basal or mid portion of the mural leaflet, leaving its distal "residual" segment in the left ventricle. Subsequently, during systole this "residual" segment approached or touched the ventricular septum. Systolic anterior motion of the mural leaflet was present in 6 (12%) of our patients with hypertrophic cardiomyopathy. Lengthening of the leaflet and an abnormal coaptation were associated with increased thickening of the posterior wall of the left ventricle and narrowing of the left ventricular outflow tract. All these elements contribute to the occurrence of systolic anterior motion and left ventricular tract obstruction.
Genesis of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an anatomical or dynamic event?
To determine the relative role of both the anatomical and dynamic components involved in the determination of systolic anterior motion (SAM) of the mitral valve, we studied 53 selected patients with hypertrophic cardiomyopathy (HCM) by M-mode and cross-sectional echocardiography (CSE). Recordings of high quality for quantitative analysis were a precondition for the inclusion in the study. Twelve of these patients had no SAM, 14 had SAM of the anterior mitral leaflet (AML), six had SAM of the posterior mitral leaflet (PML), and 21 had SAM of both the AML and PML. The length of both the AML and PML, the left ventricular outflow tract (LVOT) area and the percentage of thickening of the left ventricular posterior wall (%LVPW) were measured in 18 control subjects (group I), in patients with AML-SAM (group II), in patients with AML+ PML-SAM (Group III), in patients with PML-SAM (group IV) and in patients with HCM but without SAM (group V). The length of AML in group I (23 +/- 1.5 mm) was significantly different compared with that in groups III (28 +/- 2 mm) and IV (29 +/- 2 mm), P less than 0.001. Significant differences were present in the PML-length between group I (14 +/- 1 mm) and groups III (20 +/- 3 mm) and IV (25 +/- 4 mm), respectively (P less than 0.001), between group II (14 +/- 2 mm) and groups III and IV, respectively (P less than 0.001), and also between group V (14 +/- 1 mm) and groups III and IV (P less than 0.001). Differences were found when the %LVPW of groups II (76 +/- 17%), III (77 +/- 11%) and IV (83 +/- 19%) were compared, respectively, with groups I (42 +/- 12%) and V (54 +/- 7%), P less than 0.001; a significant difference was also found between groups I and V, P less than 0.001. The mean LVOT area was significantly reduced in groups II (3.5 +/- 1.3 cm2), III (3 +/- 1 cm2) and IV (3 +/- 1 cm2) when compared with group V (5.9 cm2), P less than 0.001. We conclude that the induction and maintenance of SAM in HCM is multifactorial, mainly depending on the length of both the AML and/or PML, the LVOT area and on the increased contractility of the LVPW.
Surgical coronary reperfusion during acute myocardial infarction.
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Doppler and two-dimensional echocardiographic observations of systolic anterior motion of the mitral valve in d-transposition of the great arteries: an explanation of the left ventricular outflow tract gradient.
Echocardiographic demonstration of systolic anterior motion of the mitral valve was seen in a 17 year old patient after the Mustard operation for d-transposition of the great arteries with intact ventricular septum. An increased flow velocity was measured by continuous wave Doppler echocardiography in the left ventricular outflow tract corresponding to an estimated peak gradient of 46 mm Hg. The presence of such a gradient had been shown earlier by the postoperative cardiac catheterization.
Acute mitral insufficiency.
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Myocardial salvage by surgical therapy in impending or evolving myocardial infarction.
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Acute evolving myocardial infarction. A surgical emergency.
This is a report of 342 cases of acute evolving myocardial infarction treated with prompt coronary artery bypass. Myocardial infarction results from a time-related sequence of ischemic pathophysiological changes. The first hours constitute a rapidly progressive event. Prompt surgical revascularization partially prevents impending myocardial necrosis; occasionally it may even prevent it completely. The results are limited infarct size, decreased mortality and morbidity, and a striking absence of the complications associated with conventional therapy (ventricular aneurysm or perforation and septal and papillary muscle rupture).
Problems faced by new directors of internal medicine residencies.
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Changes in regional myocardial blood flow and variable development of hypertrophy after aortic banding in puppies.
Supravalvar aortic banding was performed in 6 to 12 week puppies. Sixteen animals were studied 7.3 (3.5 to 10) months later, closed-chested under morphine-chloralose, catheters being positioned in the great vessels and heart, including the left atrium for microsphere injection. Compared with 11 controls, eight dogs developed biventricular hypertrophy, four isolated left ventricular hypertrophy and four had no hypertrophy. The left ventricular systolic pressure was similar (P greater than 0.05) in these 3 banded groups (mean, 30 +/- 2 [SEM] kPa, [222 +/- 16 mmHg], n = 16). The left ventricle was divided into three coronal slices with approximately 59 samples being taken from subendocardial, midwall, and subepicardial layers and additional samples from the atria and right ventricle for regional myocardial flow measurement. As left ventricular hypertrophy increased, the subendocardial/subepicardial flow ratio decreased (r = -0.8). Heterogeneity of left ventricular regional myocardial flow, including a base-to-apex decrease in flow, present in controls, was markedly reduced in the banded dogs. Analysis of variance was found to be the most sensitive test for detecting left ventricular perfusion abnormalities since in banded dogs without hypertrophy, total and regional subendocardial/subepicardial flow ratios were not significantly different from control values, whereas the subendocardial circumferential flow pattern determined by analysis of variance was significantly different from control in these dogs (P less than 0.05).
Critical care medicine. Certification as a multidisciplinary subspecialty.
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Immediate coronary artery bypass for acute evolving myocardial infarction.
Two hundred twenty-seven consecutive patients had chest pain and electrocardiographic, coronary angiographic, ventriculographic, and retrospective enzyme changes consistent with acute evolving myocardial infarction (AEMI). These patients underwent coronary artery bypass grafting an average of less than 6 hours after the start of chest pain. The mean age was 55.8 years (range 28 to 79 years). Sex, coronary artery involvement, and preoperative and postoperative enzymes and electrocardiograms are presented. Follow-up angiocardiograms done an average of 12.7 months postoperatively revealed 99 patent primary grafts in 102 patients (94.3%). Ejection fractions were normal, unchanged, or improved in 86.3% of the patients. Two ventricular aneurysms measuring less than 2.5 cm in diameter were noted. Surgical in-hospital mortality was 1.76% and first-year mortality was 1.44%. Conventional therapy in 200 AEMI patients treated at the same hospitals resulted in an in-hospital mortality of 11.5%. Follow-up of 213 patients having coronary artery bypass grafting revealed that 14% had mild angina. AEMI interrupted by coronary artery bypass grafting early in the syndrome yields results which are superior to conventional management.
Surgical management of acute myocardial infarction.
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Left atrial transport function.
These studies show that the left atrial booster pump action serves as a supercharger which can increase left ventricular stroke volume in the range of 25 percent; and in patients with aortic stenosis, stroke work in the range of 50 percent (4). These changes can occur in the face of increased resistance to left ventricular filling in clinical conditions such as aortic stenosis where there is diminished left ventricular compliance and in mitral stenosis where there is stenotic resistance to left ventricular filling from the atrium. In spite of this fact, assessment of left atrial function by measurement of cardiac output changes occurring after return from atrial fibrillation to normal sinus rhythm yields erratic and confusing results. The reason for this is that atrial function, per se, is not a primary determinant of steady state cardiac output. Sequential A-V pacing may temporarily increase stroke volume in an acute setting like myocardial infarction. Nevertheless, one cannot infer from such observations that the use of permanent transvenous A-V sequential pacing will augment steady state cardiac output over a period of time. This is an important point to remember when considering the use of sequential A-V pacing, since it requires insertion of more complicated pacing and sensing wires as well as a more complex circuitry. All of these features lead to an increased risk of pacemaker malfunction. This increased risk of malfunction is not justified unless there is good evidence that atrial contribution is important in a given patient.
The Bezold reflex: a special case of the left ventricular mechanoreceptor reflex.
Our previous finding that increasing myocardial contractility caused reflex systemic hypotension, the left ventricular (LV) mechanoreceptor reflex, suggested that the classical Bezold reflex (systemic hypotension and bradycardia after intracoronary administration of veratrum alkaloids) may be initiated by these same LV mechanoreceptors. In our working LV preparation with the coronary and systemic circulations isolated and perfused separately, intracoronary injection of veratrum alkaloids, like that of catecholamines or ouabain, had a positive inotropic effect which produced the hypotensive response typical of the LV mechanoreceptor reflex. To test directly if veratridine's positive inotropic effect initiates the Bezold reflex, verapamil, which blocks the slow Ca(2+) channels of myocardial cells but leaves intracardiac nerves unaffected, was injected by the intracoronary route to prevent the increased contractility from intracoronary injection of veratridine which also abolished the reflex hypotension, demonstrating conclusively that increasing myocardial contractility and thereby activating LV mechanoreceptors but not chemoreceptors initiates the Bezold reflex. Contrariwise, decreasing contractility or cardiac asystole by administration of tetrodotoxin, verapamil, or EDTA resulted in an increase in the systemic resistance, indicating that changes in the magnitude of the stimulus initiating the LV mechanoreceptor reflex (i.e., changes in myocardial contractility) lead to directionally opposite changes in peripheral resistance, as in the sino-aortic mechanoreflexes. Thus, it is concluded that the Bezold reflex is a special case of the LV mechanoreceptor reflex. The latter, by means of feedback mechanisms, functions normally by continuously matching the peripheral resistance to the LV contractile state so as to maintain the arterial pressure constant, thereby playing an important role in blood pressure regulation.