Biomedical subjects
Publications and source records attributed to W C Little.
The performance of the heart is regulated by the level of myocardial contractility and the cardiac preload and afterload. These factors, previously of interest primarily to basic scientists, are now clinically important for an understanding of both cardiac function and therapeutics. In this brief review, the essence of these concepts is summarized and related to the treatment of cardiac failure.
We report our experience with the use of a standard left Amplatz coronary catheter and a guidewire to cross the aortic valve in 34 patients being evaluated for valvular aortic stenosis. A number of 2 Amplatz left coronary catheter inserted via the femoral artery was positioned above the noncoronary aortic valve cusp with the tip aligned toward the aortic valve. This catheter allowed a soft-tipped, Teflon-coated guidewire to be guided through the aortic valve orifice. The catheter was then advanced over the guidewire into the left ventricle. This technique was successful within six minutes in 32 of 34 patients (94%). The stenotic aortic valve was crossed in less than two minutes in 15 patients (42%) and in less than four minutes in 31 (91%). The aortic valve was not crossed in two patients. Twenty-one patients (62%) had an aortic valve area of less than 0.75 cm2. There were no complications. We conclude that this technique provides a method for safe, rapid transaortic left ventricular catheterization in patients with aortic stenosis of all degrees of severity.
To assess the ability of biplane cineangiography in the diagnostic evaluation of acute dissection of the aorta, 20 patients with acute dissection were studied within 24 hours of surgery or autopsy, or both. Biplane large film aortic angiography was performed in 11 patients (Group I) and biplane aortic cineangiography in 9 (Group II). The morphology of the aortic valve was defined precisely in 5 (50 percent) of 10 patients in Group I and in all 9 patients (100 percent) in Group II (p less than 0.02). Aortic regurgitation weas diagnosed in all patients in both groups in whom it was present (p = not significant). Intimal tears were localized in 5 (50 percent) of 10 patients in Group I and in 8 (89 percent) of 9 in Group II (p less than 0.07). Intimal flaps were not identified angiographically in three patients in Group I and were identified in four patients (100 percent) in Group II (p less than 0.01). The presence of retrograde dissection was established in three (38 percent) of eight patients in Group I and in four (100 percent) of four patients in Group II (p less than 0.05). There was no difference in the ability to identify a nonclotted false lumen between cine and large film angiography. It is concluded that in addition to improved diagnostic capabilities, technical advantages make cineangiography a good alternative to large film angiography in the diagnostic evaluation of patients with acute dissection of the aorta.
A 25 year old woman with effort intolerance and systemic venous congestion since childhood, and restrictive ventricular filling and severe atrioventricular (A-V) valve regurgitation at cardiac catheterization died after valve replacement surgery. At autopsy, the atria were enlarged and thickened; both ventricles were small. In some areas the right ventricular wall was only a few myofibers thick. The myofibers of both ventricles were hypertrophied, and there was widespread fiber disarray in the left ventricular free wall, the interventricular septum and, focally, the right ventricular free wall. Because the ventricles were not enlarged or thickened despite myocardial fiber hypertrophy and severe chronic A-V valve regurgitation, and the myofiber disarray was widespread, this is a very unusual case of biventricular hypoplasia and dysplasia.
Cardiac catheterization in a patient 4 weeks after coronary arterial bypass surgery demonstrated the typical hemodynamic findings of constrictive pericarditis, which completely resolved after removal of 500 ml of clotted pericardial blood. The pericardium was not responsible for the findings because it was left in place. This case demonstrates that clotted hemopericardium may mimic constrictive pericarditis.
Morphologic changes in the subendocardial myocardium that appeared to be caused by severe, chronic subendocardial ischemia were studied in patients with fatal ischemic heart disease admitted to the Specialized Center of Research for Ischemic Heart Disease at the University of Alabama in Birmingham in the period 1970--1977. Thirteen patients were selected for this report on the basis that they had the lesions in the subendocardial myocardium we believe to have been caused by subendocardial ischemia and had no evidence of acute or remote myocardial infarction or other conditions that may have contributed to their terminal illness or death. Clinical findings were unstable angina, congestive heart failure, usually no increase in plasma enzymes indicative of myocardial damage, and electrocardiographic changes consistent with subendocardial ischemia. All 13 patients had 75% or greater stenosis of the three major coronary arteries; none had acute thrombotic or embolic coronary artery occlusion. The left ventricle in all cases was hypertrophied. The subendocardial myocardium showed circumferential pallor, hyperemia, or focal fibrosis without perceptible loss of volume in papillary muscles or trabeculae carneae. Microscopically, acute lesions showed one to two layers of preserved myofibers adjacent to the endocardium, vacuolar change in the deeper fibers, and focal areas of coagulation necrosis of variable size in the myocardium external to the fibers with vacuolar change. Coagulation necrosis was extensive in some cases and usually was not associated with infiltration of neutrophils. The repair reaction involved removal of necrotic sarcoplasm by mononuclear phagocytes, resulting in a reticular-appearing tissue without evidence of stromal collapse. Granulation tissue was not seen. Collagen fibers appeared to be deposited within the area of previous sarcolemmal sheaths. The distribution and morphology of subendocardial myocardial lesions associated with severe coronary atherosclerosis are distinctive and can be distinguished from myocardial necrosis or fibrosis associated with acute total occlusion of a coronary artery.
A young woman ingested approximately 13 gm of an over-the-counter acetaminophen preparation and died seven days later in profound coma. Postmortem findings included massive centrilobular hepatic necrosis and renal tubular necrosis. Although hepatotoxicity secondary to acetaminophen overdose is well recognized in Britain, this entity has received little emphasis in the United States. Recognition of the potentially severe consequences is important because early treatment with sulfhydryl compounds may prevent serious liver injury.
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Diastole can be divided into four phases: isovolumic relaxation, early filling, diastasis, and atrial systole. The amount of LV filling that occurs during each of these phases depends on myocardial relaxation, the passive characteristics of the LV, the characteristics of the left atrium, pulmonary veins, and mitral valve, and the heart rate. When diastolic function is normal, the net effect of these factors results in an LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics. Invasive studies can quantitate the rate of myocardial relaxation and the LV diastolic pressure-volume relation. More recently, RNA and Doppler echocardiography have been used to noninvasively evaluate diastolic performance by determining the pattern of LV diastolic filling. At rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients who do not have clinically apparent diastolic dysfunction and in normals. Furthermore, a normal pattern can occur in patients who have severe diastolic dysfunction. A reduced early diastolic filling, in the absence of pulmonary congestion, indicates the loss of diastolic reserve, since the left atrium is being used as a booster pump. This pattern of diastolic filling in a patient who has symptoms of pulmonary congestion may suggest diastolic dysfunction, even if the systolic LV performance is normal. Since diastolic filling of the LV results from a complex interplay of factors, it is unlikely that a single, easily interpreted index of LV diastolic performance will ever be developed. However, the recent development of a noninvasive evaluation of the pattern of LV diastolic filling by RNA or Doppler echocardiography is an important advance. When interpreted with an understanding of the determinants of LV filling and the patient's clinical status, these noninvasive tests can contribute to the rational assessment of LV diastolic performance.
Although the S3 gallop sound has long been used clinically as an indicator of left ventricular systolic dysfunction, the mechanism responsible for its production remains controversial. The same sound is often found in young healthy individuals, and whether a similar mechanism is responsible is also unknown. The relationship of the S3 gallop sound to the dynamics of left ventricular filling was compared in 18 healthy young triathletes and 15 older subjects with cardiac disease. Twenty healthy normal subjects without an S3 were included as controls. Phonocardiographic, two-dimensional echocardiographic, and Doppler echocardiographic analysis of left ventricular inflow were evaluated. The S3 in both groups always occurred close to peak early filling velocity (E), during early flow deceleration. Mean E deceleration rate was higher in the subjects with S3 (726 +/- 153 cm/sec2 in the triathletes and 819 +/- 274 cm/sec2 in those with cardiac disease) than in control subjects (563 +/- 131 cm/sec2, p less than 0.001 in both cases). Ten triathletes underwent examination both before and immediately after 30 degrees head-up tilt. E deceleration rate dropped significantly with head-up tilt (720 +/- 137 vs 590 +/- 174 cm/sec2, p less than 0.01), while concurrently the S3 disappeared or was diminished in amplitude. Similar changes were seen in subjects with cardiac disease. We conclude that both the "pathologic" and "physiologic" S3 are related to abnormally rapid deceleration of early diastolic left ventricular inflow. Although the presence of the S3 is not dependent on the state of left ventricular systolic function, diastolic filling is characterized by a predominance of early inflow with a rapid flow deceleration rate.