Cellular and molecular pathways to myocardial necrosis and replacement fibrosis.

Fibrosis is a fundamental component of the adverse structural remodeling of myocardium present in the failing heart. Replacement fibrosis appears at sites of previous cardiomyocyte necrosis to preserve the structural integrity of the myocardium, but not without adverse functional consequences. The extensive nature of this microscopic scarring suggests cardiomyocyte necrosis is widespread and the loss of these contractile elements, combined with fibrous tissue deposition in the form of a stiff in-series and in-parallel elastic elements, contributes to the progressive failure of this normally efficient muscular pump.

Myocardial remodeling in low-renin hypertension: molecular pathways to cellular injury in relative aldosteronism.

The pathologic hypertrophy of hypertensive heart disease is related to the quality, not the quantity, of myocardium; the presence of fibrosis is inevitably linked to structural and functional insufficiencies with increased cardiovascular risk. Elevations in plasma aldosterone that are inappropriate relative to dietary sodium, or relative aldosteronism, are accompanied by suppressed plasma renin activity, elevation in arterial pressure, and dyshomeostasis of divalent cations. The accompanying hypocalcemia, hypomagnesemia, and hypozincemia of aldosteronism contribute to the appearance of secondary hyperparathyroidism.

Coupled calcium and zinc dyshomeostasis and oxidative stress in cardiac myocytes and mitochondria of rats with chronic aldosteronism.

A dyshomeostasis of extra- and intracellular Ca(2+) and Zn(2+) occurs in rats receiving chronic aldosterone/salt treatment (ALDOST). Herein, we hypothesized that the dyshomeostasis of intracellular Ca(2+) and Zn(2+) is intrinsically coupled that alters the redox state of cardiac myocytes and mitochondria, with Ca(2+) serving as a pro-oxidant and Zn(2+) as an antioxidant. Toward this end, we harvested hearts from rats receiving 4 weeks of ALDOST alone or cotreatment with either spironolactone (Spiro), an aldosterone receptor antagonist, or amlodipine (Amlod), an L-type Ca(2+) channel blocker, and from age/sex-matched untreated controls.

Causes and consequences of zinc dyshomeostasis in rats with chronic aldosteronism.

Iterations in Ca2+ and Mg2+ balance accompany aldosteronism (inappropriate for dietary Na+ intake). Increased Zn excretion and Zn translocation to injured tissues, including the heart, also occurs. Several causes and consequences of Zn dyshomeostasis in rats receiving aldosterone/salt treatment (ALDOST) were examined.

Bilateral pleural effusions in congestive heart failure.

The salt-avid state that accounts for the clinical syndrome congestive heart failure (CHF) leads to an initial expansion of intra- and subsequent rise in extravascular volumes that can include the appearance of pleural effusion. Herein, we present a 54-year-old man with a dilated cardiomyopathy who was hospitalized because of his CHF, which included bilateral pleural effusions, right hydrothorax greater than left. The pathophysiology of pleural fluid formation in CHF, previously debated, has now reached consensus, albeit not frequently reviewed.