Left ventricular cellular hypertrophy in pressure- and volume-overload valvular heart disease

To determine the dependence of myocyte hypertrophy in chronic valvular heart disease on the site and type of lesion, the myocardium was studied from 11 patients with either pressure-overload hypertrophy (PO; four patients with aortic stenosis and two with mixed aortic stenosis/insufficiency) or pure volume-overload hypertrophy (VO; two patients with mitral regurgitation and three with aortic insufficiency). These patients, all without coronary artery disease, died zero to 34 days after valve replacement surgery. Diameters of 25 longitudinally oriented myocytes in the circular midwall myocardium were measured with a calibrated light microscope eyepiece reticle on each of five transmural, transverse, histologic sections from the apical, anterolateral, posterolateral, anteroseptal, and posteroseptal left ventricle. Statistical analysis by modified two-way analysis of variance (ANOVA) demonstrated that mean myocyte size (based on 125 measurements) varied widely among cases but was not statistically different among sites. The myocyte diameter for PO lesions (25.9 +/- 1.1 micron, mean +/- SEM) was significantly greater (P less than 0.05) than that for pure VO lesions (20.4 +/- 0.7 micron), despite equal relative heart weights (measured/predicted from body weight: 2.5 +/- 0.2 [mean +/- SD] versus 2.5 +/- 0.5). This study suggests that 1) cellular hypertrophy in valvular heart disease occurs uniformly throughout the left ventricular myocardium; and 2) mean myocyte diameters are greater in PO than in VO hypertrophy for equivalent cardiac enlargement.     

Myocardial hypertrophy of the left ventricle during familial arterial hypertension

In patients with familial arterial hypertension and their relatives preclinical signs of myocardial hypertrophy were observed before the formation of stably increased blood pressure. We evaluated echocardiographic sings of left ventricular myocardial hypertrophy in normotensive relatives of patients with arterial hypertension. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 140, No. 12, pp. 625–626, December, 2005     

Left ventricular assist devices as bridge to heart transplantation in congestive heart failure with pulmonary hypertension

Severe pulmonary hypertension (PH) has been considered a significant contraindication to cardiac transplantation. Ongoing clinical experience, however, has shown that temporary support using left ventricular assist devices (LVADs) in these patients can result in significant reductions in PH. A comprehensive review of the available literature regarding the use of LVADs in heart failure patients with PH was conducted. The existing literature to date supports the use of LVADs in heart failure patients with PH and demonstrates that significant reductions in PH in these patients can be achieved. This subsequently allows for safe and effective cardiac transplantation in patients who were previously excluded from this modality. For heart failure patients with severe PH, the use of LVADs can provide significant benefits by significantly reducing PH and allowing subsequent staged transplantation.     

Left atrial receptors in arterial baroreflex control of heart rate

We have studied the influence of left atrial receptor stimulation on arterial baroreflex control of heart rate with a view to determine the role of cardiac efferent sympathetic and parasympathetic pathways in any interaction observed. Experiments were performed on anaesthetized, artificially ventilated, and thoracotomised cats and dogs. The sensitivity of baroreflex heart rate response was found to be higher in dogs as compared to cats. Both the sympathetic and parasympathetic effects contributed to the reflex chronotropic effects observed during changes in mean arterial blood pressure. The reflex tachycardia response during left atrial receptor stimulation was more pronounced in dogs than in cats. Stimulation of left atrial receptors caused slight inhibition of the baroreflex tachycardia response and potentiation of the bradycardia response.     

What's new in cellular cation exchange and humoral factors in primary hypertension?

In essential hypertension abnormalities of cellular Na+ and Ca++ handling have been described. The latter disturbance probably offers an explanation for the increased vasoconstriction in essential hypertension. The etiology of those disturbances in cellular Na+ and Ca++ metabolism may be related to genetic disturbances of membrane transport, or to a humoral factor influencing cellular cation metabolism.     

Endothelial cell activity in experimental hypertension. Effects of hemodynamic factors

The cause of the increased endothelial cell proliferative activity found in experimental hypertension in the rat is not clear. In this experiment the part played by altered vascular hemodynamics was explored in a model in which part of the aorta was subjected to a high blood pressure and the other not. Hypertension was produced by the application of a tight ligature to the aorta between the levels of the two renal arteries, the mechanism being interference with the blood supply to the more distally placed kidney. Because the aorta is constricted, the segment above the ligature is subjected to high blood pressure and the segment below it to lowered pressure, although both segments are exposed to humoral factors such as renin and angiotensin II. Aortic endothelial cells were labeled with tritiated thymidine and cell replication and cell density studies carried out using en face monolayer preparations of endothelium. It was found that endothelial cell replication was considerably increased at 7 days following induction of hypertension in segments of aorta above the ligature but not in the segment below the ligature. The increased activity was short-lived and had returned to normal levels at 4 weeks. Cell density was increased above the ligature at both 1 and 4 weeks following induction of hypertension. The changes are consistent with the idea that the increased cell replication and consequent increased cell density above the ligature were initiated by the increased stretching of the aortic wall attending the development of hypertension.     

Intimal hyperplasia and hemodynamic factors in arterial bypass and arteriovenous grafts: a review

Stenosis at the graft–vein junction caused by intimal hyperplasia (IH) is the major cause of failure of vascular access grafts used for hemodialysis. There is a strong relationship between hemodynamic factors and formation of IH. The hemodynamic pattern and the location of IH are different in arterial bypass grafts (ABGs) compared with arteriovenous grafts (AVGs). In an ABG, end-to-side anastomosis of the expanded polytetrafluoroethylene graft and artery produces hemodynamic changes around the junction. IH develops at the arterial floor and the toe and heel of the distal anastomosis. Low shear stress and oscillating shear forces at the arterial floor and the heel plus a high wall sheer stress (WSS) gradient at the toe probably promote IH development. Compliance mismatch between the graft and artery causes turbulence that may contribute to IH formation. The blood flow rate in AVGs is 5–10 times greater than that in ABGs. High flow causes turbulence that injures endothelial cells and eventually results in IH. The peak WSS in AVGs is about 6N/m², much higher than that in ABGs. Excessively high WSS may effect IH formation in AVGs. Several venous cuff or patch anastomotic designs have been used in attempts to regulate hemodynamic factors in grafts. In ABGs, these designs appear to help decrease IH formation. In AVGs, however, they generally have not improved patency rates. In a high-flow system such as an AVG, more drastic changes in anastomotic design may be required.     

Vascular remodeling process in reversibility of pulmonary arterial hypertension secondary to congenital heart disease

Pulmonary vascular remodeling process was analyzed using morphometry in lung biopsy specimens taken from 26 children, aged 6 to 160 months, who had congenital heart disease and significant pulmonary arterial hypertension. Reparative surgery was performed in 22 patients and palliative surgery was performed in four patients. One patient expired postoperatively and four others after hospital discharge. Vascular remodeling examination revealed a characteristic pathological picture: pronounced medial thickening with increased collagen content (fibrosis), without significant arterial intimal proliferation. At a mean follow-up of 44 months, 72% of the survivors were asymptomatic with no medication. Diagnosed by echocardiogram, 22% of these patients were shown to have pulmonary arterial hypertension. The characteristic pathological features described above occurred in 38% of the patients who either expired or had pulmonary hypertension postoperatively. These findings were an aid to identifying a high risk group in which the outcome does not meet expectations for the classical grade I and II changes. We concluded that the presence of isolated medial thickening does not ensure either survival or a normal postoperative pulmonary arterial pressure at late follow-up and that the collagen content can be a better reference for good outcome. Early intracardiac repair is recommended before the development of significant medial fibrosis.     

Left ventricular hypertrophy in daily dialysis

Cardiac hypertrophy, a well-known independent risk factor for cardiovascular death, is a very frequent complication in ESRD patients. Its frequency tends to be even higher in dialyzed patients due to the fact that the current dialytic treatments are unable to keep under a satisfactory control the various responsible factors and particularly the blood pressure, which is largely the most important. Daily hemodialysis, a more frequent schedule consisting of 6-7 sessions/week lasting 2 or more hours, has definitely proved its superiority in controlling blood pressure and in improving anemia, and thus has the requisites for positively influencing cardiac hypertrophy. In fact, a series of studies, both retrospective and prospective, performed during the last years by our group, have confirmed that this new, more frequent and thus more physiological schedule, is able not only to stop the progression of the cardiac hypertrophy in uremic patients but also to revert toward the normality, in a relatively short time. This appears to be essentially a consequence of the excellent blood pressure control, which in turn derives from the easier control of the true dry weight, achievable with this type of dialytic treatment.     

Cerium oxide nanoparticles attenuate monocrotaline induced right ventricular hypertrophy following pulmonary arterial hypertension

Cerium oxide (CeO₂) nanoparticles have been posited to exhibit potent anti-oxidant activity which may allow for the use of these materials in biomedical applications. Herein, we investigate whether CeO₂ nanoparticle administration can diminish right ventricular (RV) hypertrophy following four weeks of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). Male Sprague Dawley rats were randomly divided into three groups: control, MCT only (60 mg/kg), or MCT + CeO₂ nanoparticle treatment (60 mg/kg; 0.1 mg/kg). Compared to the control group, the RV weight to body weight ratio was 45% and 22% higher in the MCT and MCT + CeO₂ groups, respectively (p < 0.05). Doppler echocardiography demonstrated that CeO₂ nanoparticle treatment attenuated monocrotaline-induced changes in pulmonary flow and RV wall thickness. Paralleling these changes in cardiac function, CeO₂ nanoparticle treatment also diminished MCT-induced increases in right ventricular (RV) cardiomyocyte cross sectional area, β-myosin heavy chain, fibronectin expression, protein nitrosylation, protein carbonylation and cardiac superoxide levels. These changes with treatment were accompanied by a decrease in the ratio of Bax/Bcl2, diminished caspase-3 activation and reduction in serum inflammatory markers. Taken together, these data suggest that CeO₂ nanoparticle administration may attenuate the hypertrophic response of the heart following PAH.     

Selenium and vitamin E in relation to risk factors for coronary heart disease.

Fasting blood samples taken from 116 apparently healthy men aged 30-50 years were assayed for selenium, glutathione peroxidase activity, vitamin E, cadmium, lead, glucose, lipids, and albumin. Blood pressure was measured in each subject, and details of height, weight, smoking habits, and alcohol consumption were recorded. Multivariate analysis of the data showed that the decrease in blood and serum concentrations of selenium and the increase in whole blood cadmium concentrations in the cigarette smokers was independent of alcohol consumption. There was no correlation between blood selenium concentrations or glutathione peroxidase activities and the risk factors for cardiovascular disease. Neither alcohol consumption nor smoking had an effect on the vitamin E concentrations. There was a strong association, however, between vitamin E and serum lipid concentrations, although the increase in triglyceride concentrations in the smokers was not matched by a comparable increase in vitamin E. The possible role of selenium in the aetiology of heart disease remains unresolved.