Structural Changes In Heart Research Articles

Obesity-associated hypertension

The association of obesity and hypertension is characterized hemodynamically by an increase in absolute circulating intravascular volume that induces increased cardiac output and total peripheral resistance that remains inappropriately normal. These changes constitute the hemodynamic basis for the increase in blood pressure in obesity. Obesity-associated hypertension is also characterized by an abnormal renal response, including increased renal blood flow and a rise in glomerular and interstitial pressures. These hemodynamic changes induce the following structural changes in the heart: enlarged left atrial, ventricular and aortic root diameters as well as increased posterior septal wall thickness and left ventricular mass. The hemodynamic changes in the kidneys generate higher glomerular volume and increased interstitial infiltrate, which may cause compression of the tubules and blood vessels of the renal medulla. Weight reduction is an effective tool in the control of blood pressure, and significantly reduces the metabolic and hemodynamic derangements that occur with obesity. However, since weight reduction compliance is difficult to maintain, pharmacological agents are often needed to control blood pressure. Angiotensin-converting enzyme inhibitors, calcium channel blockers and alpha- adrenergic blocking agents may be the most appropriate therapy for obesity-associated hypertension since they intervene with some of the previously described pathophysiological conditions.

Effects of obesity and weight loss on left ventricular mass and relative wall thickness: survey and intervention study

Objectives: To investigate the consequences of longstanding obesity on left ventricular mass and structure and to examine the effects of weight loss on these variables.Design: Cross sectional survey and controlled...

Structural and left ventricular histologic changes after implantable LVAD insertion

Long-term support on the implantable left ventricular assist device (LVAD) produces structural changes in the recipient's heart. To assess the possibility of heart "recovery" we reviewed the records of 19 HeartMate LVAD recipients to determine structural and left ventricular histologic changes during LVAD support. Intraoperative transesophageal echocardiographic studies were performed in the operating room before LVAD insertion, immediately after LVAD insertion, and at explantation and heart transplantation (mean duration of support, 76 +/- 34 days). The initiation of LVAD pumping led to an immediate decrease (p < 0.001) in left ventricular dimensions, which were not significantly different by the time of device explantation. Left ventricular fractional shortening did not significantly improve during LVAD support (0.07 +/- 0.03 before LVAD; 0.11 +/- 0.10 immediately after LVAD; 0.11 +/- 0.11 before explantation). Histologic specimens showed a significant reduction in the number of wavy fibers, and contraction band necrosis (p < 0.01), both markers of acute myocyte damage. However, myocardial fibrosis increased (p < 0.05). Myocyte diameter increased slightly (p = 0.07). We conclude that implantable LVAD support is associated with immediate changes in ventricular structure. Histologic markers of acute myocyte damage improve, but fibrosis increases. Because the structural changes occur immediately, they do not indicate "recovery" of left ventricular function, but merely changes in loading conditions.

The carbamate insecticide ZZ-Aphox induced structural changes of gills, liver, gall-bladder, heart, and notochord of Rana perezi tadpoles.

Embryos of Rana perezi were kept under laboratory conditions and treated with carbamate ZZ-Aphox at chronic doses of 0.02% and 0.14% for 9 weeks. Both the histological study and the analysis of mortality show a direct relationship between the dosage and the effects of the pesticide. The histological study of the survivors over 56 days show damages in gills, liver, gall-bladder, heart, and notochord. Damages on the epithelial of gills (on their distal portion) and gall-bladder recover over a few days, whereas those provoked on the compacting of the hepatic parenchyma and the hepatocytes, the auricle and the perintocohordal collagenic fibers alter their structure in a lasting way. Potentials of such alterations are discussed, with special reference to the possible interference of the pesticide on the successful synthesis of the supporting connective sheaths.

Cavitation bioeffects: Spin-offs from lithotripsy.

Lithotripter fields can produce cavitation in the organs of the body at pressure amplitudes significantly lower than those required to fragment stones. Because of limits on the expansion of the gaseous nuclei imposed by the surrounding tissue structures, cavitation in tissue is qualitatively different from that described by classical cavitation theory for a spherical bubble in an infinite fluid. Thresholds for structural and functional changes in kidney, liver, lung, heart, and blood, developmental effects in the embryo/fetus, and killing of Drosophilia larvae have been determined. Studies of the biological effects of shock waves generated by lithotripters have guided us in the search for effects of diagnostically relevant pulsed ultrasound. In particular, lung hemorrhage occurs with pulsed ultrasound at acoustic pressures of the order of 1 MPa and effects on the dynamic behavior of heart tissue have been seen with single 1–10 ms pulses at pressure amplitudes of the order of 10 MPa. The effects in lung occur at temporal average intensities orders of magnitude lower than previously associated with biological effects in mammals.

Physiological Approach to Future Developments in Therapy

First, the multifactorial background of primary hypertension is outlined in principle, where particular attention is given to the early, sometimes even genetically reinforced structural "upward resetting" of the cardiovascular system, which soon dominates hemodynamics in both human and rat hypertension. On this basis, it is then discussed which modes of action that antihypertensive treatment could best achieve regression of the structural changes in heart and vessels. Since both the luminal and wall changes can be affected in a different manner, and since the growth processes may be reinforced by both genetic and neurohormonal "trophic" influences, there are potentially many ways by which regression could be accomplished via specific interferences, apart from the blood pressure lowering per se. As to the "hemodynamic profile" of drug interferences, reasons are given for an approach where a systemic resistance vessel dilatation is combined with a mild damping of the beta-adrenergic sympathetic drive on the heart.

Structural changes in heart and vessels during hypertension with aspects on their reversibility.

Structural changes in heart and vessels during hypertension with aspects on their reversibility.

Quantitative fine structural changes in dog heart following cardiopulmonary bypass

Quantitative analysis of electron micrographs was performed on cardiac biopsies obtained before and approximately I h following hypothermic cardiopulmonary bypass at 28°C. During bypass the myocardium was exposed to 5, 20 and 30 min of ischemia. Alterations in mitochondrial structure were seen after only 5 min of myocardial ischemia and consisted of end-to-end fusion of these organelles. In the control biopsies, mitochondrial volume fraction ( V vi ) was 0.25, but after 5 min of aortic occlusion it increased to 0.38; after 20 min it was 0.40 and some mitochondria were mildly swollen. After 30 min, V vi was 0.31 and some giant mitochondria were disrupted. The reduction in V vi at 30 min may have been due to the appearance of a new population of small spherical mitochondria. Function studies were done before and after bypass. Mean maximal left ventricular power after 5, 20 and 30 min of myocardial ischemia at 27°C was decreased to 86, 68 and 59%, respectively, of that observed before bypass. This study shows that disruption of myocardial organelles occurs following 20 to 30 min of hypothermic ischemia, corresponding with the moderate decrease in maximal LVP at 30 min.

Experimental Chronic Hypertension in the Rat: Structural Changes in Blood Vessels, Heart and Kidneys

SummaryVarying degrees of chronic hypertension were produced in 16 rats by application of a figure-of-eight ligature to one or both kidneys. The animals were killed after the blood pressure had been maintained between levels of 150 to 240 mm of mercury for periods varying from 1 to 8 months. Microscopic examinations disclosed in each animal a marked cardiac hypertrophy particularly of the left ventricle. Renal lesions apparently responsible for the hypertension were observed in every kidney to which a ligature was applied and focal lesions of a slight degree apparently due to the hypertension were observed in the opposite intact kidney. No pertinent changes of any degree were seen in the large or small arteries of the organs examined.