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Background: Although 50% of hypertensive patients in the community are estimated to have diastolic dysfunction, there is no specific guideline for diastolic dysfunction therapy at present despite the condition's clear association with increased cardiovascular risk. Although the efficacy of angiotensin II receptor blockers (ARBs) in hypertension and left ventricular hypertrophy regression has been established, the effect of angiotensin II receptor blockade on intrinsic parameters of diastolic function has not been evaluated in large-scale studies., Methods: The VALIDD Trial is an investigator-initiated randomized, controlled, double-blind clinical trial on approximately 350 patients designed to explore whether antihypertensive therapy with the ARB valsartan, in addition to standard therapy, would improve intrinsic diastolic properties of the myocardium in patients with hypertension and evidence of diastolic dysfunction. The result of such therapy will be compared with placebo after 38 weeks of treatment. The primary efficacy variable is change in early diastolic lateral mitral annular relaxation velocity measured by tissue Doppler imaging on week 38., Conclusions: We expect the VALIDD Trial to provide novel insights into the specific effects of ARBs on diastolic dysfunction, as assessed by tissue Doppler imaging, in hypertensive patients. The trial may provide clinically useful data on whether such therapy can directly improve diastolic function in patients with hypertension.

We investigated the incidence and mechanism of pulmonary artery hypertension (PAH) in a consecutive series of patients with aortic stenosis who were undergoing diagnostic cardiac catheterization. Forty-five patients with severe aortic stenosis were divided into two groups: group 1 comprised 13 patients (29%) with PAH (pulmonary artery systolic pressure > 50 mm Hg); group 2 comprised 32 patients (71%) without PAH. Group 1 patients had a higher incidence of congestive heart failure, a lower left ventricular ejection fraction and cardiac index, and more mitral regurgitation as compared with group 2 patients. Of the 13 group 1 patients, 8 had a transpulmonary gradient (pulmonary artery mean pressure--pulmonary capillary wedge pressure) > or = 10 mm Hg, consistent with reactive PAH. We conclude that PAH frequently accompanies aortic stenosis and is often reactive.

The diagnosis of myocardial contusion is often difficult, as traditional methods such as serial electrocardiograms, cardiac enzyme (creatine kinase [CK-MB]) analysis, and echocardiography lack sensitivity and specificity. Recent reports have shown that 111In labelled antimyosin scanning has high sensitivity for detecting cardiac injury. However, no prior studies have been reported for antimyosin imaging with patients suspected of sustaining a cardiac contusion. Accordingly, 17 patients with severe multisystem trauma (intrathoracic vascular injury in eight patients, pneumothorax and pulmonary contusion in 13) underwent antimyosin scintigraphy, echocardiography, 12-lead electrocardiograms, and CK-MB determinations. Arrhythmias were noted in seven patients, four of whom died. All patients has elevated CK levels but CK-MB isoenzyme was greater than 4% in only three. Abnormal ST segments were noted in nine subjects, only one of whom had CK-MB elevation. Echocardiography revealed pericardial effusions in four patients but was technically suboptimal in 53% of the studies. Blinded interpretation of the antimyosin scans revealed only one with focal myocardial uptake; this same patient had the only discrete wall motion abnormality on the echocardiogram and also had ST depression with ectopy but normal CK-MB. Thus in patients with suspected myocardial contusion, echocardiography is frequently limited technically and the electrocardiogram and CK analysis appear to lack diagnostic accuracy. In contrast, monoclonal antimyosin imaging may be performed in patients with trauma without limitation and yields results that are concordant with echocardiograms. In patients with suspected myocardial contusion, focal antimyosin uptake is uncommon despite severe thoracic injury, which suggests that extensive myocardial necrosis is not the primary method of injury.

To determine how frequently new wall-motion abnormalities that are indicative of ischemia accompany thallium redistribution, 47 consecutive patients underwent two-dimensional echocardiography during routine dipyridamole-thallium stress testing. A secondary aim of the study was to determine whether the addition of isometric handgrip exercises to the standard dipyridamole imaging protocol increased the frequency of wall-motion abnormalities or thallium redistribution. Echocardiograms and thallium scans were independently interpreted, and wall-motion abnormalities that appeared with dipyridamole, handgrip exercise, or both were compared with results of thallium imaging. Five of 24 patients with thallium redistribution had new wall-motion abnormalities, and the extent (number of segments) of thallium redistribution in these five patients was significantly greater than in those who did not have well-motion abnormalities (p less than 0.03). The addition of isometric handgrip exercises to the imaging protocol did not distinguish between patients with and without new wall-motion abnormalities or thallium redistribution. Thus new wall-motion abnormalities infrequently accompany thallium redistribution in routine dipyridamole stress testing in spite of the addition of handgrip exercises, but when new wall-motion abnormalities are present, they are associated with a greater area of thallium redistribution.