The left atrium modulates left ventricular filling through three components: a phase of reservoir or expansion during systole, a conduit phase during diastole, and an active contractile component (when sinus rhythm is present) during late diastole. This active contractile component of the left atrium has an important role in patients with ventricular dysfunction as a 'booster pump' to augment ventricular volume. Augmented left atrial booster function is one of the mechanisms compensating for decreased early filling in patients with reduced left ventricular compliance, whereas a loss of atrial contraction, as a result of atrial fibrillation or ventricular pacing, reduces cardiac output by approximately 15-20% [1,2] .During exercise left atrial reservoir and booster functions are augmented, whereas conduit function is not; increased reservoir function may play an important role in accelerating left ventricular filling by helping to maintain an enhanced atrioventricular pressure gradient during diastole and also by increasing left atrial booster function through an increase in preload [3] . An isolated decrease in left atrial compliance is associated with relative increases in the conduit function of the left atrium. The ability to optimally redistribute left ventricular filling among reservoir, conduit and boosterpump functions is a potentially important adaptation that may occur in the left atrium in response to changing haemodynamics [4] . Frank-Starling mechanismThe stretch of the atrium was controlled by intra-atrial pressure. The Frank-Starling behaviour of the atrium was manifested as a biphasic increase of the contraction force after increasing the stretch level. The development of the contraction force after step increase of the stretch (intra-atrial pressure from 1 to 3 mmHg) was accompanied by an increase in the amplitude of the calcium transients and a decrease in the time constant of Ca 2+ transient decay. The stretch-activated channel activation led to gradual augmentation of Ca 2+ transients, which modulated the action potentials through increased Na + /Ca 2+ -exchanger inward current. The role of troponin C affinity change was to modulate the Ca 2+ transients, stabilize the diastolic [Ca 2+] i, and presumably to produce the immediate increase of the contraction force after stretch seen in experiments. The same mechanism that caused the normal physiological responses to stretch could also generate arrhythmogenic afterpotentials at high stretch levels in the model [15] .With a stepwise decrease in the pacing rate from 110 beats . min 1 to 70 beats . min 1 , the left atrial dimension increases just before atrial contraction and left atrial systolic shortening increases as well. However, the calculated left ventricular filling volume during atrial systole decreases. The pulmonary venous flow during atrial systole is directed toward the left atrium, and the left atrial influx volume from pulmonary venous flow decreases. With a decrease in the pacing rate, the left atrial Frank-Starling mechanism operates....

Abstract-Aortic stiffness may predict progression to hypertension beyond classic risk factors. In a longitudinal study, we assessed the predictive value of aortic stiffness on future hypertension in nonhypertensive subjects with blood pressure (BP) Ͻ140/90. Aortic stiffness was determined by echocardiography at baseline in 2512 subjects. The follow-up time was 4 years. A stepwise increase in hypertension incidence occurred across the male and older participants: 3.8% of young female individuals, 11.5% of young male, 26.1% of old female, and 58.8% of old male subjects progressed to hypertension over 4 years. In multivariate analysis, aortic stain, distensibility, and stiffness index (␤) remained significantly associated with the progression to future hypertension after adjustment to classic risk factors in men and women and in young and old populations. This study provides the first direct evidence to our knowledge in a longitudinal study that aortic stiffness is an independent predictor of progression to hypertension in nonhypertensive individuals. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in patients with essential hypertension. 4 -6 Furthermore, aortic stiffness constant is the best single predictor of acute coronary syndromes. 6,7 Aortic stiffness may predict sustained hypertension; in patients with hypertension and hypothyroidism and in patients with repaired coarctation of aorta, sustained hypertension is caused by the increased aortic stiffness. 8,9 The aim of the present study was to increase the reliability of prediction of future BP by using aortic stiffness in nonhypertensive subjects who were followed-up in our outpatient department. Methods Study PopulationA total of 2571 subjects (1460 women and 1111 men), aged 35 to 94 years, entered the study. This population included subjects examined in our outpatient department, and they were free of the following exclusion criteria: hypertension (systolic BP Ն140 mm Hg or a diastolic BP Ն90 mm Hg, or the use of antihypertensive medication); overt cardiovascular disease or symptoms; and history of a myocardial infarction or of congestive heart failure. None of these patients was referred for typical symptoms of coronary heart disease or other cardiovascular disease. All participants gave informed consent.Four years later, all participants were re-examined and aortic stiffness was measured again. The coexistence of metabolic or endocrine conditions affecting aortic stiffness was studied by the routine clinical examination and determination of hormones by specific laboratory tests. Some participants (239; 9.5%) started on BP-altering medication during the follow-up period. Before measurements, any medication was discontinued for at least 5 half-lives before the study. A total of 2512 subjects (1440 women and 1072 men), aged 35 to 94 years, were successfully re-examined after 4-year interval. Fifty-nine (2.3%) subjects were lost from observation. Twenty-one deaths have occurred, 11 of them caused by cardiovascular even...

CRP concentration is a risk factor for recurrent and permanent AF. Methylprednisolone successfully prevents recurrent and permanent AF.

Aortic elastic properties are compromised and energy loss due to aortic wall viscosity is increased in hypertensives compared with normotensives. Function of the aorta is improved in both hypertensive and normotensive subjects after the administration of diltiazem.