Mauro Zennaro

Influence of regression of left ventricular hypertrophy on left atrial size and function in patients with moderate hypertension

Objectives. The aim of the study was to evaluate the effect of regression of left ventricular (LV) hypertrophy on left atrial (LA) size and function in patients treated with telmisartan, an angiotensin II receptor blocker. Methods. Patients population included 80 patients with mild–moderate LV hypertrophy treated with telmisartan. Patients were followed over a period of 12 months from the start of telmisartan treatment. LA size was measured during systole from the parasternal long‐axis view from M‐mode. Atrial function was assessed by Doppler‐echocardiography and the following parameters were measured: transmitral peak A velocity, atrial filling fraction, atrial ejection force (AEF), peak E velocity, deceleration time and isovolumic relaxation time, LA maximal and minimal volume, and LV cardiac mass index (LVMI). Results. All patients had an increased LVMI and decrease during follow‐up. LA dimensions were greater at baseline and reduced after 1 year of treatment. LA volume indexes maximal volume, minimal volume and P volume were reduced compared with baseline value (maximal volume from 35±5 to 32±5, p<0.05; minimal volumes from 14±2 to 10±4, p<0.05). AEF, a parameter of atrial systolic function, increased from 12±3 to 15±2.4 (p<0.01). The reduction of LA volumes correlate with reduction of LVMI (LA maximal volume and LVMI r = 0.45; p<0.01; LA minimal volume and LVMI r = 0.34; p<0.05). A positive correlation was also found between LV mass index and P volume (r = 0.41; p<0.01), LV mass index and LA active emptying volume (r = 0.39; p<0.01), and LV mass index and LA total emptying volume (r = 0.38; p<0.05). Conclusions. The present study suggests that regression of LV hypertrophy due to telmisartan is associated with reduction of LA volumes that expresses variation of LV end‐diastolic pressure. The reduction of LV end‐diastolic pressure is associated with an increase in diastolic filling and with a significant reduction of active and passive emptying contribution of left atrium to LV stroke volume.

Heparin/PF4 antibodies formation after heparin treatment : Temporal aspects and long-term follow-up

BACKGROUND Heparin-induced thrombocytopenia is characterized by the presence of heparin-induced antibodies against heparin/platelet factor-4 (PF4) complex and paradoxical thrombosis. Little is known on the persistence of antiheparin antibodies in blood. The aim of this study was to evaluate the time course of heparin/PF4 antibodies in patients exposed to heparin. METHODS We initially enrolled 500 patients treated with unfractionated heparin as part of perioperative management of coronary artery bypass graft; those who developed serologically confirmed heparin/PF4 antibodies were selected for further follow-up. Over 3 years, we repeatedly assessed serum concentration of antibodies (by enzyme-linked immunosorbent assay) and occurrence of thrombotic events. RESULTS One hundred thirty-one patients (26.2%) developed anti-PF4/heparin antibodies, which persisted for a median time of 90 days (Quartile 1-Quartile 3, 31-186). At 30 days, patients with antibodies had higher incidence of thrombotic events (28.2% vs 14.9%, P < .01) and death/myocardial infarction (14.5% vs 7.8%, P < .001). Of the 131 patients with antiheparin/PF4 antibodies, 78 had already developed antibodies before cardiac surgery; such patients became serologically negative more slowly than patients who developed antibodies after surgery. Over 3 years of follow-up, patients with anti-PF4/heparin antibodies developed 65 thrombotic events, 25 patients developed deep vein thrombosis and/or pulmonary embolism, and 20 patients myocardial infarction. CONCLUSIONS Patients with heparin-induced antibodies are more likely to develop thrombosis after cardiac surgery. Patients in whom antibodies are present before surgery show longer persistence of antibodies and increased incidence of thrombotic events over time. Persistence of antibodies suggests that these patients may be at risk for developing thrombosis; and therefore, further exposure to heparin should be limited.

Effect of coffee consumption, lifestyle and acute life stress in the development of acute lone atrial fibrillation

Objective The study evaluated the relationships between acute stress, lifestyle and coffee consumption, and acute lone atrial fibrillation (AF). Methods The study group included 400 patients with mean age of 54 ± 11 years, 205 of whom were men. They all presented with a first episode of AF. Patients underwent a series of cognitive tests to evaluate acute psychological stress (mean life acute stress score). Lifestyle and nutritional parameters (diet, alcohol and espresso coffee consumption, smoking and obesity) were investigated. An age-matched and sex-matched control group was selected and compared. Results Recent stress, high intake of coffee, and obesity were associated with greater risk of AF. Acute stress induces an increase in coffee consumption and changes in lifestyle. The increase in coffee consumption was more marked in nonhabitual drinkers, leading to a higher risk of developing AF [odds ratio (OR) 4.1; 95% confidence interval (CI): 1.98–4.56; P < 0.001]. Spontaneous conversion of AF to sinus rhythm was observed in 191 patients (47%). Patients who experienced AF after an acute stress showed the highest probability of spontaneous conversion. High espresso coffee consumption (OR 0.86; 95% CI: 0.49–1.21; P < 0.01) and obesity (OR 0.88; 95% CI: 0.84–1.20; P < 0.01) were associated with a significantly greater risk of persistent AF. Conclusion Acute stress induced changes in lifestyle, including an increase in coffee consumption, leading to a higher risk of AF. Patients who developed AF after an acute stress showed the highest probability of spontaneous conversion. High espresso coffee consumption and obesity were associated with an increased risk of persistent AF.

Left atrial remodeling after short duration atrial fibrillation in hypertrophic hearts

trial fibrillation (AF) is the most common sustainedcardiac arrhythmia found in hypertensive patients. AFcauses atrial dilation, and progressive left atrial (LA)enlargement occurs once AF becomes chronic. In theFramingham heart study, LA enlargement was associatedboth with the duration of elevated blood pressure and withthe level of systolic pressure.