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It has been reported that older patients with hypertrophic obstructive cardiomyopathy (HOCM) benefited the most from dual chamber (DDD) pacing. Since in older patients the distribution of septal hypertrophy and left ventricular (LV) cavity shape differs from that in younger patients, we decided to study the efficacy of DDD pacing on the reduction of LV outflow tract (LVOT) gradient in different patterns of septa! hypertrophy. We compared HOCM patients with nonreversed septal curvature, thus preserving the elliptical LV cavity contour (common in the elderly), (group I) versus patients with reversed septal curvature, deforming the LV cavity to a crescent shape (common in the young), (group II). Eighteen HOCM patients were studied (11 patients in group I and 7 patients in group II). After implantation of a DDD pacemaker, the LVOT gradient was measured using Doppler echocardiography at various programmed AV delay intervals to determine the maximal percentage decrease of LVOT gradient from baseline. The measurement was repeated after at least a 6-month follow-up (chronic DDD pacing). The baseline LVOT gradient was comparable between groups (79 ± 28 vs 81 ± 25 mmHg, P = 0.92). The LVOT gradient reduction at acute DDD pacing was significantly greater in group I than group II (61 ± 18% vs 23 ± 10%, P = 0.0001). This difference in favor of the patients from group I was maintained at midterm follow-up (69 ± 17% vs 40 ± 17% P = 0.0076). In conclusion, patients with normal septal curvature and preserved elliptical LV cavity shape had a greater reduction of LVOT gradient after DDD pacing than patients with reversed septal curvature deforming LV cavity. The proposed criterion assessing the septal curvature may be useful to predict the efficacy of DDD pacing in the reduction of LVOT gradient. [ABSTRACT FROM AUTHOR]

It has been suggested that in hypertrophic cardiomyopathy (HC), vascular abnormalities are not restricted to the heart. Flow-mediated dilation of peripheral conductance arteries (reflecting their endothelial function) has not yet been studied in HC. Our aim was to assess both flow-dependent dilation of the brachial artery and flow responses (dependent on resistance vessels) during forearm reactive hyperemia (RH) in nontreated HC patients. The authors studied 13 HC patients and 14 age- and sex-matched healthy controls. None of them exhibited any factors known to be associated with endothelial dysfunction. Using 7 MHz ultrasound, brachial artery diameter and Doppler flow velocity were measured continuously at baseline and throughout 1 min of RH following 5 min of forearm ischemia induced by inflation of a blood pressure cuff. Arterial diameter and RH flow are expressed as percent changes with respect to the baseline. Flow-dependent dilation was similar in the HC patients and control subjects (7.2 ±9.5% vs 9.9 ±10.4%, p>0.05). Compared to the control group, RH flow in HC was decreased; however, differences did not reach statistical significance until 60 sec of RH (112 ±102% vs 261 ±217%, p<0.05; HC vs controls). In HC patients, endothelial function of peripheral conductance arteries is preserved. Hence, a defect in the forearm arterial bed in HC seems to be limited to mechanisms maintaining the dilation of resistance vessels during decreasing RH flow. [ABSTRACT FROM AUTHOR]

Aortic stenosis (AS) represents the most common type of acquired valvular heart disease. Its incidence increases with age; therefore, from 3% to 9% of adults over 75 years of age develop AS. The pathophysiological mechanisms and role of biomarkers in the prediction of AS have been extensively studied. Progression of AS is characterized by a number of abnormalities in calcification regulation, inflammation/adipokine dysregulation, prothrombic state, and altered von Willebrand factor function. The current understanding of the mechanisms of AS involves a complex role of the multiple cell types, in particular myofibroblasts and macrophages. The introduction of transcatheter aortic valve implantation provides invaluable opportunities for periprocedural and long-term monitoring of the changes in the biomarker profile. Effective pharmacological treatment, especially in the early stage of AS, is largely unknown. The current review discusses not only the pathophysiology of AS but also attempts at pharmacological treatment.

Introduction: Studies conducted so far have shown that patients with left ventricular hypertrophy have increased adiponectin levels; however, these studies were performed only in resting condition., Objectives: The aim of the study was to compare adiponectin, resistin, and leptin levels (at rest and after exercise) between patients with hypertrophic cardiomyopathy (HCM) and healthy controls. Additionally, we examined potential relationships between the levels of the 3 adipokines and the left ventricular outflow tract (LVOT) gradient both at rest and at peak exercise., Patients and Methods: We studied 29 patients with HCM (mean age 42.7 ±11.9 years, 16 men and 13 women). The control group included 19 healthy subjects matched for age-, sex-, and the body mass index. After echocardiographic examination in a supine position, all patients were placed in an upright position and treadmill exercise test was performed with simultaneous continuous echocardiographic monitoring of the LVOT gradient. Adiponectin, resistin, and leptin levels were measured immediately prior to exercise in a supine position and at peak exercise in an upright position., Results: At baseline (at rest), adiponectin levels tended to be increased in patients with HCM (P = 0.09), while resistin and leptin levels were significantly higher in patients with HCM than in healthy controls. In HCM patients, exercise induced an increase in adiponectin (20.74 ±7.95 vs. 22.52 ±8.10 μg/ml, P <0.05), a decrease in leptin (22.78 ±6.08 vs. 20.63 ±5.57 ng/ml, P <0.05), and no significant effect on resistin. In the control group, all biomarkers mildly decreased at peak exercise (adiponectin 19.23 ±5.43 vs. 18.66 ±5.31 μg/ml P = 0.044), resistin 14.80 ±1.87 vs. 13.87 ±1.21 ng/ml, P = 0.030), (leptin 14.34 ±4.74 vs. 13.50 ±3.98 ng/ml, P = 0.045). In HCM patients, neither resting nor peak exercise values of the LVOT gradient correlated with any levels of adipokines., Conclusions: In patients with HCM, but not in healthy individuals, moderate exercise induced an increase in adiponectin levels and a decrease in leptin levels independent of a rise in the LVOT gradient. The potential cardioprotective role of adiponectin during exercise stress in HCM requires further studies.

In chronic hypertension, autoregulation of cerebral blood flow (CBF) is adapted to high blood pressure. Thus in untreated hypertensive patients, the autoregulation curve is shifted towards higher pressure. With antihypertensive treatment autoregulation curve may be shifted back to the normal position or shift upward to the beneficially higher level of CBF. The effect of various antihypertensive drugs on CBF has been discussed.