Improvement in midwall myocardial shortening with regression of left ventricular hypertrophy.

Despite normal indices of left ventricular (LV) chamber function, patients with LV hypertrophy (LVH) due to hypertension are thought to have depressed midwall systolic shortening compared with normotensives. The aims of the present study were (1) to confirm this observation and (2) to assess the effects of antihypertensive therapy that cause regression of LVH on LV systolic function assessed at both the midwall and endocardium. Thirty-eight previously untreated hypertensive subjects with LVH underwent echocardiography and were compared with 38 normotensive control subjects. Comparisons between the group with LVH and the control group revealed no significant differences in cardiac output (4. 32+/-0.23 versus 4.55+/-0.21 L/min), ejection fraction (62.5+/-2% versus 66.4+/-1.07%), or endocardial fractional shortening (34.5+/-1.45% versus 37.0+/-0.82%), but shortening assessed at the midwall was significantly less in the group with LVH (17.9+/-1.11% versus 21.6+/-0.63%, P<0.01). Subsequently, 32 patients with uncontrolled hypertension (24 previously untreated and 8 on existing antihypertensive therapy) underwent treatment with ramipril, with the addition of felodipine and bendrofluazide if required, to reduce blood pressure to <140/90 mm Hg. These 32 patients underwent echocardiography at baseline, after blood pressure control, and after an additional 6 months of tight blood pressure control. Good blood pressure control was achieved after 6 months compared with baseline (143/86+/-2.8/1.4 versus 174/103+/-4.1/1.9 mm Hg; P<0.01) with significant regression of LV mass index (124+/-3.4 versus 145+/-3.8 g/m(2), P<0.01). LV fractional shortening assessed at the midwall improved with regression of LVH (21.9+/-0.84 and 18.7+/-1. 19%, P<0.05), with posttreatment midwall shortening being similar to that of the normal control subjects evaluated in the first study. Hypertensive patients with LVH have depressed midwall systolic shortening despite normal indices of LV chamber function. Regression of LVH after good blood pressure control improved midwall shortening to normal levels.

Cardioversion of atrial arrhythmias: audit of anticoagulation management.

Patients undergoing cardioversion for chronic atrial fibrillation should receive anticoagulation for three weeks before and four weeks after the procedure. Patients with atrial flutter and acute atrial fibrillation are also at risk of thromboembolic complications, so they too should be anticoagulated for cardioversion. Of the 36 acutely admitted patients who were cardioverted, 18 were in atrial fibrillation and 18 in atrial flutter. All except three of those in fibrillation were anticoagulated with heparin before cardioversion, but only seven received warfarin after cardioversion. Of those in flutter, 10 received heparin and eight received no anticoagulation before cardioversion. One patient underwent transoesophageal echocardiography before cardioversion to exclude atrial thrombi. Only two patients received warfarin for a month after cardioversion. Of the 20 elective cardioversions, 10 were in atrial fibrillation and 10 in atrial flutter. Five of those in fibrillation had received at least three weeks' treatment with warfarin before cardioversion and two underwent transoesophageal echocardiography; the other three received either up to two hours of heparin or no anticoagulation before cardioversion. Only five patients received warfarin for a month after cardioversion. Nine of those in flutter received a few hours of heparin before cardioversion and one was not anticoagulated; none underwent transoesophageal echocardiography or received warfarin after cardioversion. The results of this audit demonstrate that anticoagulation for atrial arrhythmias was inconsistent and often inadequate. A formal anticoagulation policy for cardioversion has now been adopted.

Vascular network changes in the retina with age and hypertension.

OBJECTIVE: To compare retinal arterial bifurcation geometry in normotensive and hypertensive subjects. DESIGN: A retrospective observational study. METHODS: Fluorescein angiograms of normotensive (n = 13) and hypertensive (n = 12) subjects aged 30-80 years with uni-ocular retinal pathology were compared. Quantification of diameters of the parent, larger daughter and smaller daughter vessels (d0, d1 and d2, respectively) and of bifurcation angles (the angle between the two daughter arterioles, omega) of arteriolar bifurcations was performed from digitized retinal angiograms of the uninvolved eye. The relative diameters of parent and daughter vessels at bifurcations were summarized by junction exponents (x) such that d1x + d2x = d0x. RESULTS: Junction exponents were similar for normotensives and hypertensives (means +/- SEM, 2.65 +/- 0.18 and 2.48 +/- 0.17), but analysis of covariance showed a parallel decrease in x in the two groups with age. A positive association was found between x and arteriolar microvascular density. Bifurcation angles were more acute in hypertensives (74 +/- 3 degrees) than in normotensives (84 +/- 3 degrees) and declined with increasing age in both groups. CONCLUSIONS: The present findings indicate that ageing and possibly hypertension are associated with disadvantageous branching geometry in the human retinal vasculature, implying increased power costs of blood transport, uneven distribution of shear forces throughout the vascular tree and microvascular rarefaction. The present findings may have important implications for our understanding of the pathogenesis of vascular disease in ageing and hypertension and offer the prospect of a novel sensitive diagnostic approach to the cardiovascular system.