Influenceof left ventricular hypertrophy on ventricular arrhythmias in hypertensive patients.
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Abstract:
Objectives：Left ventricular hypertrophy(LVH) increases the risk of sudden death in hypertensive patients and this is known due to ventricular arrhythmias. Thus, author studied the relationship between LVH as a hypertensive target organ damage and ventricular arrhythmias.
Methods：24-hour ambulatory electrocardiographic monitoring, measurement of microalbumin in 24-hour urine and fundoscopic examination were performed on 100 hypertensives (50 patients without LVH and 50 patients with LVH on EKG) who admitted Pusan National University Hospital.
Results：In patients with LVH, ventricular extrasystoles occurred more frequently than without LVH(p<0.05) and ventricular couplet and ventricular tachycardia were more common but statistically not different. Microalbuminuria and hypertensive retinopathy were more severe in patients with LVH than without LVH(p<0.05 and p<0.01, respectively). Conclusion：Of the ventricular arrhythmias, ventricular extrasystole but not ventricular couplet and ventricular tachycardia occurred more frequently in patients with LVH than without LVH. Thus, prospective study with long-term follow up should be done to establish the relationship between hypertensive LVH and cardiovascular mortality, especially sudden death. And, further study should be done to make the relationship between reduction in LVH with antihypertensive therapy and reduction in LVH-associated ventricular arrhythmias.Keywords:
Hypertensive retinopathy
Microalbuminuria
Sudden Death
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There is little information on left ventricular (LV) hypertrophy (LVH) development during antihypertensive treatment. We evaluate incident LVH in a treated hypertensive cohort, the Campania Salute Network registry. We analyzed prospectively 4290 hypertensives (aged 50.3±11.1 years, 40% women) with at least 1-year follow-up, without LVH at baseline. Incident LVH was defined as the first detection of echocardiographic LV mass index ≥47 in women or ≥50 g/m2.7 in men. During a median 48-month follow-up, 915 patients (21.3%) developed LVH. They were older, more frequently women, and obese (P<0.0001), with initial higher fasting glucose, diastolic and systolic blood pressure, LV mass index, lower heart rate and glomerular filtration rate, longer hypertension history and follow-up, and higher average systolic blood pressure during follow-up (all P<0.05), despite a more frequent treatment with Ca++-channel blockers and diuretics (both P<0.02). At multivariable Cox regression, incident LVH was independently associated with older age, female sex, obesity, higher average systolic blood pressure during follow-up, and initial greater LV mass index (all P<0.02). By categorizing patients according to obesity and sex, obesity independently increased the risk for incident LVH in both sexes (obese versus nonobese men: hazard ratio, 1.34; confidence interval, 1.05-1.72; P=0.019; and obese versus nonobese women: hazard ratio, 1.34; confidence interval, 1.08-1.66; P=0.007). Despite more aggressive antihypertensive therapy, 21% of hypertensive patients develop clear-cut LVH. After adjusting for confounders, risk of incident LVH is particular relevant among women and is further increased by the presence of obesity.URL: http://www.clinicaltrials.gov. Unique identifier: NCT02211365.
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Abstract BACKGROUND Electrocardiographic (ECG) left ventricular hypertrophy (LVH) is a strong predictor of cardiovascular (CV) morbidity and mortality. However, the predictive value of ECG LVH in treated hypertensive patients remains unclear. METHODS A total of 33,357 patients (aged ≥ 55 years) with hypertension and at least 1 other coronary heart disease (CHD) risk factor were randomized to chlorthalidone, amlodipine, or lisinopril. The outcome of the present study was all-cause mortality; and secondary endpoints were CHD, nonfatal myocardial infarction (MI), stroke, angina, heart failure (HF), and peripheral arterial disease. Cornell voltage criteria (S in V3 + R in aVL > 28 [men] or >22 mm [women]) defined ECG LVH. RESULTS ECGs were available at baseline in 26,384 patients. Baseline Cornell voltage LVH was present in 1,741 (7%) patients, who were older (67.4 vs. 66.6 years, P < 0.001), more likely to be female (74 vs. 44%, P < 0001) with a higher systolic blood pressure (151 vs. 146 mm Hg, P < 0.001) than patients without ECG LVH. During 5.0 ± 1.4 years mean follow-up, baseline and in-study ECG LVH was significantly associated with 29 to 98% increased risks of all-cause mortality, MI, CHD, stroke, and HF in multivariable Cox analyses. CONCLUSIONS Baseline Cornell voltage LVH is associated with increased CV morbidity and all-cause mortality in treated hypertensive patients independent of treatment modality and other CV risk factors. CLINICAL TRIALS REGISTRATION Trial Number NCT00000542.
Amlodipine
Stroke
Chlorthalidone
Hypertensive heart disease
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Indapamide
Perindopril
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Left ventricular hypertrophy (LVH) is an early complication of hypertension. To a certain degree, this process counteracts the parietal stress induced by high blood pressure. Genetic factors, obesity, high salt diet and different growth factors, notably angiotensin II and noradrenaline, can also predispose to hypertrophic cardiomyopathy. Left ventricular mass is increased on echocardiography in about 20% of hypertensive subjects. LVH is initially associated with a change in myocardial diastolic function and later with abnormal systolic function. It is a major risk factor, a cause of cardiac failure, reduction in coronary reserve and of ventricular arrhythmias. Treatment of hypertension is associated with regression of LVH and preservation or improvement in myocardial diastolic and systolic functions. The decrease in left ventricular mass could reduce the incidence of cardiovascular complications in hypertension.
Pathophysiology
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Hypertensive heart disease
Supraventricular arrhythmia
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Echocardiography provides a relatively simple, non-invasive, reproducible means of assessing left ventricular hypertrophy (LVH). Evidence has accumulated both from animal and clinical studies that LVH occurs quite early as a cardiac response to hypertension and indeed occurs at a greater frequency (40–50% of mild to moderate cases) than had been previously anticipated by electrocardiographic studies (2–5%) of similarly hypertensive patients. Recent studies also indicate that LVH can regress, with appropriate drug therapy, within a relatively short interval of time, but whether or not this is accompanied by reversal of vascular hypertrophy or by salubrious or adverse effects of ventricular function and coronary blood flow is not established. A variety of antihypertensive medications have been studied in an effort to reverse LVH. It appears that drugs which inhibit catecholamines, e.g., α2-agonists, converting enzyme inhibitors and ß-blocking agents, are capable of reducing LVH at least in many patients. On the other hand, drugs which increase catecholamines, such as diuretics and direct vasodilators, appear to have no beneficial effect on LVH in spite of satisfactory reductions in blood pressure.
Ventricular hypertrophy
Coronary vasodilator
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Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.
Essential hypertension
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