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At least 739 records · Page 41Linked to original sources
PubMed1970

Value of reference tracings in diagnosis and assessment of constrictive epi- and pericarditis.

Reference tracings are of great value in the diagnosis and assessment of constrictive pericarditis. The Q-h interval in the jugular venous pulse tracing is strongly correlated with the mean right atrial pressure (r=0.91). The left ventricular ejection time, the Q-A2 interval, and the Q-h interval are independent during atrial fibrillation from the preceding diastolic filling interval. This differentiates constrictive pericarditis from valvular heart disease. Cases with haemodynamically significant constrictive epicarditis are characterized by a rapid evolution, absence of pericardial calcification and absence of an early diastolic filling sound, a dominant a wave in the jugular venous pulse tracing, and a high early diastolic ventricular pressure. The haemodynamic behaviour is similar to that found in cases with myocardial fibrosis.

Adolescent↗
PubMed1993

Structural basis for pathologic left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a major risk factor associated with the emergence of symptomatic congestive heart failure. Cardiac myocyte excitation-contraction coupling has been the biochemical focus in the search for insights into the impaired contractility, relaxation, and stiffness of the hypertrophied myocardium. Although hypertrophied myocytes are the hallmark of LVH, other aspects of myocardial structure may be altered to impair pump function--specifically an abnormal accumulation of connective tissue (interstitial fibrosis). Cardiac fibroblasts, which are nonmyocyte cells of the cardiac interstitium, synthesize and degrade collagen and, therefore, represent an important determinant of pathologic LVH. Significantly, this reactive fibrosis has been found not only in the pressure-overloaded hypertrophied left ventricle but also in the normotensive, nonhypertrophied right ventricle of animals with experimental hypertension. These findings suggest the involvement of a circulating substance that has access to the coronary circulation common to both ventricles. Based on in vivo studies that examined this hypothesis, it can be concluded that chronic elevation of circulating aldosterone, relative to sodium intake, is associated with myocardial fibrosis, which initially adversely alters diastolic function and ultimately systolic ventricular function. The mechanisms by which fibroblast collagen metabolism is invoked in this setting are under investigation. Elucidation of these mechanisms may prepare the way to the prevention as well as the reversal of myocardial fibrosis and, in turn, of pathologic LVH.

Animals↗
PubMedDate not supplied

Isolated noncompaction of the ventricular myocardium.

Isolated noncompaction of the ventricular myocardium is a recently described anomaly. We report the first case of this anomaly presenting as a restrictive cardiomyopathy, and the first association of this entity with endocardial fibrosis.

Cardiomyopathy, Restrictive↗
PubMed1993

[From myocardial hypertrophy to heart failure: role of the interstitium].

In the progression from myocardial hypertrophy to heart failure, abnormalities in the interstitial space of the heart seem to play a critical role. The formation of an extracellular oedema and the alterations in coronary subendocardial perfusion are associated with the development of interstitial fibrosis. Cardiac experimental studies documented the presence of augmented interstitial fluid volume and pressure and a subsequent remodelling of the fibrillar network of the extracellular space of the myocardium during the phases of the cardiovascular response to a sudden overload. Variations of the Starling's forces balance caused by enhanced endothelial permeability or due to an impairment of cardiac lymphatic drainage may contribute to the development of an acute heart failure. During stable hyperfunction, the organization of a chronic oedema should account for interstitial changes in the hypertrophic myocardium. Reactive fibrosis seems to be under hormonal control. The activation of the renin-angiotensin-aldosterone system is responsible for interfascicular and intercellular accumulation of fibrillar collagen within the cardiac interstitium. Perivascular fibrosis in the subendocardium may impair intramyocardial distribution of coronary flow. When an inadequate hypertrophy occurs, because of an elevation in ventricular wall stress, myocardial oxygen consumption rises and this may lead to the exhaustion of coronary blood flow reserve in the subendocardial layers. This underperfusion may be responsible for the development of myocardial ischemia. Coronary hemodynamic changes in the microcirculation as those prompted by interstitial alterations may contribute to the onset of myocyte necrosis and to the formation of restorative fibrosis. The progressive mechanical overload of the spared hypertrophied myocytes could explain the initiation of a positive feedback mechanism which perpetuates endomyocardial perfusion impairment, interstitial oedema and remodelling, finally, causing myocyte deaths and fibrous tissue proliferation. These structural alterations and their pathophysiological counterparts appear to be closely related to the evolution from compensatory hypertrophy to chronic myocardial failure in hypertrophic heart disease.

Acute Disease↗
PubMed1991

Extreme axis deviation in a Nigerian with severe congestive cardiac failure: an unusual manifestation.

A case of severe congestive cardiac failure of unidentified etiology demonstrating an extreme electrical QRS axis is presented. The axis is about -120 degrees. This electrocardiographic manifestation is rare, and, to the best of our knowledge, there have been no previously reported cases in congestive cardiac failure in our environment. This finding, in view of the clinical state of our patient, may be indicative of extreme severity resulting in widespread patchy myocardial fibrosis.

Cardiomyopathy, Dilated↗
PubMed2006

[Cardiac alterations caused by renal failure].

Cardiac disease is the most common cause of death in patients with endstage renal disease. It was assumed that the high rate of cardiovascular mortality was based on accelerated atherosclerosis. Recently published articles, however, demonstrated that only 30-50% of all cardiac deaths in patients with uremia was due to myocardial infarction. On the other hand 30-40% of all patients with renal insufficiency, angina pectoris and documented ischemia have normal coronary arteries. Therefore, it is suggested that in patients with chronic uremia apart from accelerated atherosclerosis further abnormalities of the heart lead to myocardial ischemia. Recently published papers report functional and structural changes, which affect myocardial perfusion reserve. These structural changes include left ventricular hypertrophy, interstitial myocardial fibrosis, and microvascular disease.

Cause of Death↗