Platelet activation in embolic and preembolic status of patients with nonrheumatic atrial fibrillation.

STUDY OBJECTIVE: Information on platelet activation possibly associated with a preembolic or embolic status in nonrheumatic atrial fibrillation (AF) with special regard to the role of platelet membrane activation markers (P-selectin and CD63). STUDY POPULATION: The study included 60 patients with nonrheumatic AF; 28 of them had a history of an embolic event. The age-matched control group consisted of 28 healthy subjects (13 men and 15 women). INTERVENTIONS: Patients underwent transesophageal echocardiography to detect eventual intracardiac thrombus or spontaneous echo contrast that would represent a preembolic status. Blood samples were taken from all persons to evaluate markers for platelet activation under these conditions. RESULTS: Measurements of hematologic variables did not differ significantly between normal subjects and patients presenting with AF but no preembolic or embolic status. Elevated concentrations of fibrinogen were significantly related to the presence of left atrial spontaneous echo contrast. The amount of circulating platelets expressing P-selectin and CD63 was significantly higher in the patients positive for both spontaneous echo contrast and left atrial thrombus or embolic events. Furthermore, in these groups, significantly more leukocyte-platelet conjugates were present. CONCLUSION: Platelet activation indicated by platelet membrane activation markers occurs in embolic and preembolic status of patients with nonrheumatic AF.

Regression of left ventricular hypertrophy in hemodialysis patients is possible.

Regression of left ventricular hypertrophy in hemodialysis patients is possible. Left ventricular hypertrophy represents the major risk factor for cardiac morbidity and mortality. Therefore, their regression is mandatory. Since the causes of uremia-associated left ventricular hypertrophy are multifactorial, various therapeutic options can be considered: optimal control of arterial hypertension and volume status, optimal correction of metabolic acidosis, best possible correction of hypoalbuminemia and severe secondary hyperparathyroidism, modern pharmacotherapeutic strategy for the treatment of heart failure (use of angiotensin-converting enzyme inhibitors in combination with angiotensin II receptor blockers and beta-blockers) and total correction of renal anemia. Following the proposed therapeutic strategies we could, by using echocardiography, distinguish in 100 hemodialysis patients the following 3 groups (on the average after 1.5 years): 36 patients with initially normal left ventricular mass index (LVMI (g/m2), F < 110; M < 130) maintained normal (group 1); in 31 patients with moderately increased LVMI full regression resulted (group 2); 33 patients with severely increased LVMI (group 3) had to be further divided into 2 sub-groups: 22 patients with significant improvement of LVMI, 11 patients with no, regression. For the first time we were able to show that it is possible to maintain initially normal LVMI during long-term treatment and to achieve complete regression and significant improvement of LVMI in our patients. However, since LVMI requires a long time to develop, a similarly long time must be estimated for its regression. However, 11 patients remained therapeutically resistant. In this group, severe heart diseases were often combined and highly prevalent, including ischemic heart and valve diseases and end-stage dilatative cardiomyopathy. These patients had to be transferred to cardiac surgery. Anemia is considered to be one of the most important factors for the development of left ventricular hypertrophy. Therefore, total correction of renal anemia has to be strongly recommended in addition to other measures of our therapeutic strategy to maintain full or significant regression of left ventricular hypertrophy.