Relations of serum aldosterone and microalbuminuria to left ventricular hypertrophy in patients with essential hypertension

Left ventricular hypertrophy [LVH] is an independent risk factor for cardiovascular morbidity and mortality in hypertensive patients. The identification of risk factors for the initiation of LVH in patients with hypertension [HTN] is important including microalbuminunuria [MAU] and hyperaldosteronism. Evaluation of the relationship of MAU and plasma aldosterone to blood pressure [BP] and LVH in patients with essential HTN. Thirty male patients with essential HTN and 15 healthy subjects as a control group were subjected to thorough clinical examination, transthoracic echocardiography, lipid profile, serum potassium, and serum aldosterone estimation. MAU was evaluated with dipstick Micral-II Test of fasting midstream morning urine on two successive days. Left ventricular mass index [LVMI] was calculated and values >134gm/m[2] were considered as LVH. Patients with LVMI >134 gm/m[2] had higher serum aldosterone, BMI, Interventricular septal thickness [IVST], Posterior wall thickness [PWT] and Relative wall thickness [RWT]. Serum aldosterone was significantly higher among the test hypertensive group and was positively correlated correlated with LVMI, RWT, PWT, IVST, LVM and negatively correlated with LV diastolic dimensions. MAU was positively correlated with systolic BP, Pulse pressure, BMI and LVMI and a strong relationship between MAU and serum aldosterone was detected. Aldosterone is an important contributor to the development of LVH and hypertensive nephropathy and strong relation between microalbuminuria and aldosterone is detected. The Value of selective aldosterone blockers in preventing target organ damage [TOD] awaits further investigation

Effect of acute cerebrovascular stroke on QT dispersion

Background: Repolarization and ischemic-like electrocardiographic [ECG] changes observed during acute phase of stroke may cause diagnostic and management dilemmas for the clinician. Some of these changes have been thought to be due either to the stroke state itself or pre-existing heart disease

Objective: The aim of this study is to assess the effect of acute phase of stroke on QT dispersion [QTd]

Patients and Methods: The study consisted of 42 patients [24] males and [18] females [test group], hospitalized for acute cerebrovascular stroke within 24 hours of symptom onset. A control group of 38 healthy presons were submitted to the study. They were age and sex matched. All test and control groups were subjected to history taking, clinical examination especially cardiac and neurological examination, routine laboratory tests, echocardiography. Twelve leads ECG was done for both test group and control group during the first 24 hours after symptom onset then after one week for test group. Norepinephrine level was done for both test and control groups

Results: QT dispersion and corrected QT dispersion [QTcd] were significantly greater in 24h-ECG than in 1 week [1w] ECG and the control ECG [P < 0.001]. In 24h-ECG QTd and QTcd were significantly greater in patients with larger lesions [mean +/- SD [0.048+/-0.009 and 0.053 +/- 0.009] vs small lesions [0.04 +/- 0.009 and 0.041+0.004] seconds, P < 0.001]. In 1w-ECG patients with right sided lesions were found to have significantly greater QTd and QTcd values [[0.034+0.008 and 0.039+0.005] vs left sided lesions [0.025+0.007 and 0.03+0.004] seconds, P< 0.001]

Conclusion: Acute stroke increases QTd and QTcd in patients without any known cardiac diseases. In the first 24hour, QTd and QTcd seem to be more prominent and related to humoral effects of acute insult. However, within one week, stroke localization may also play a role