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Left Ventricular Hypertrophy Predicts Outcome of Hypertension Regardless of the Type of Ventricular Arrhythmia Present

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Left Ventricular Hypertrophy Predicts Outcome of Hypertension Regardless of the Type of Ventricular Arrhythmia Present Journal of Human Hypertension (1999) 13, 617–623 1999 Stockton Press. All rights reserved 0950-9240/99 $15.00 http://www.stockton-press.co.uk/jhh ORIGINAL ARTICLE Left ventricular hypertrophy predicts outcome of hypertension regardless of the type of ventricular arrhythmia present C de C Frimm, BM Trezza, C Gruppi, CCJ Medeiros, M Cu´ ri and EM Krieger Heart Institute, School of Medicine, University of Sa˜ o Paulo, Brazil Left ventricular hypertrophy is associated with an survived, those dying from cardiovascular causes had increased cardiovascular mortality in hypertension. A a greater percentage of electrocardiographic left ven- -and coup (0.0037 ؍ potential role of ventricular arrhythmias is debated but tricular hypertrophy (83 vs 36%, P .(0.0467 ؍ not yet determined. The purpose of this study was to lets of ventricular ectopic beats (58 vs 18%, P evaluate whether the presence of arrhythmias would In addition, they showed larger left ventricular diastolic ascribe any additional risk to cardiovascular mortality diameter (60 ؎ 10 vs 53 ؎ 8 mm), mass index (248 ؎ 67 beyond that related to the presence of left ventricular vs 154 ؎ 57 g/m2) and posterior wall thickness (12 ؎ 2 -hypertrophy. From November 1988 to February 1991, 40 vs 10 ؎ 2 mm), as well as shorter left ventricular frac mild to severe hypertensive patients (mean SBP, DBP tional shortening (0.23 ؎ 0.8 vs 0.32 ؎ 0.9). Univariate 183/117 mm Hg) were submitted to clinical, echocardio- analysis showed that electrocardiographic left ventricu- graphic and electrocardiographic evaluations com- lar hypertrophy and strain, mass index, end-systolic plemented by 24-h Holter monitoring and then followed wall stress, fractional shortening and the presence of until November 1996. The Kaplan–Meier method sup- couplets were significantly related to cardiovascular plemented by the Cox multiple regression model were mortality. However, only mass index was shown to be performed to identify the variable(s) associated with independently associated with cardiovascular death. In fatal cardiovascular outcome. Twelve cardiovascular conclusion, left ventricular hypertrophy predicts cardio- fatalities occurred as a consequence of sudden death vascular outcome, regardless of the presence of other -and myocar- signs of cardiac damage, including ventricular arrhyth (2 ؍ heart failure (n ,(4 ؍ stroke (n ,(4 ؍ n) .In comparison with patients who mia .(2 ؍ dial infarction (n Keywords: hypertrophy; arrhythmias; cardiovascular mortality; echocardiography; Holter Introduction mias, as opposed to left ventricular hypertrophy, in cardiovascular mortality of patients with hyperten- Hypertension has long been recognised as one of the sion. main risk factors for cardiovascular morbidity and mortality. More recently, data obtained from the Fra- mingham Heart Study have revealed a significant Material and methods association between left ventricular hypertrophy All procedures were carried out in accordance with and cardiovascular fatalities, an association inde- 1 institutional guidelines and the protocol was pendent of blood pressure levels. In addition, sev- approved by our institutional review committee. eral studies have reported an increased prevalence Between November 1988 and February 1991, 43 of hypertensive patients with asymptomatic ven- patients with mild to severe essential hypertension tricular arrhythmias associated with the presence 2–4 were selected and gave informed consent for and the degree of left ventricular hypertrophy. entering the study. Patients underwent complete However, it has not yet been determined whether an clinical and biochemical evaluations, including cas- increase in either frequency or complexity of ven- ual blood pressure determinations. Patients with a tricular arrhythmias is related to a fatal outcome in suggestive history of ischaemic heart disease, valvu- hypertensive subjects, such as the relationship 5,6 lar heart disease, diabetes, alcohol abuse, renal fail- shown in patients with ischaemic heart disease ure with creatinine levels above 2 mg/dl and other 7,8 and hypertrophic cardiomyopathy. The present metabolic diseases were excluded. Antihypertensive long-term prospective study was undertaken to drugs were withdrawn 2 weeks before enrolment in evaluate the particular role of ventricular arrhyth- 33 patients to avoid hypothetical interference of antihypertensive therapy on cardiac rhythm. Clini- cal status of the remaining 10, all with severe hyper- Correspondence: Clovis de Carvalho Frimm, Heart Institute, School of Medicine, University of Sa˜o Paulo, Av. Dr. Eneas de tension, including four patients with a previous Carvalho Aguiar, 44 05403-900 - Sa˜o Paulo, SP, Brazil history of congestive heart failure, precluded Received 20 May 1999 the interruption of antihypertensive treatment for Hypertension: hypertrophy, arrhythmias and outcome C de C Frimm et al 618 ethical reasons. Neither one of them, however, was ventricular tachycardia, characterised as Ͼ3 con- receiving beta-blockers, digitalis or angiotensin- secutive ventricular ectopic complexes occurring at converting enzyme inhibitors before the study. After a rate of Ͼ100 beats/min. The frequency of Ͼ10 ven- completing Holter monitoring, the medications were tricular ectopic beats per hour was selected based restarted. Basically, a diuretic (hydrochlorothiazide) on the observations showing that at this rate the was the first drug employed, followed by an adre- mortality of a postinfarction population reaches a nergic inhibitor (methyldopa or propranolol) and a plateau.15 Multiform ventricular ectopic beats and vasodilator (hydralazine). Potassium supplements, R-on-T complexes were not contemplated, since potassium-sparing diuretic (amiloride), angiotensin- they were shown to have little significance on prog- converting inhibitors and loop diuretics were added nosis.16 as necessary. Patients with frequent or complex ventricular All patients underwent standard 12-lead electro- arrhythmias who gave informed consent were sub- cardiogram. Electrocardiographic left ventricular mitted to coronary angiography to rule out a signifi- hypertrophy and strain were established based on cant (Ͼ70%) coronary artery obstruction that could the presence voltage criteria SV1 + RV5 Ͼ3.5 mV likely imply the rhythm disturbances to myocar- and ST depression of у0.05 mV associated to T- dial ischaemia. wave inversion of у0.1 mV in leads I, aVL and V5 Cardiovascular mortality was selected as the end- or V6. point of the study. The causes of fatalities occurring outside our institution were determined with the help of a metropolitan database system on mortality Echocardiographic study in Sa˜o Paulo and further substantiated by phone or M-mode two-dimensionally guided tracings were personal contacts with first degree relatives. The cir- obtained using an ALOKA SSD 870 equipment and cumstances of sudden deaths (up to 1 h after the 2.5 and 3.5 MHz transducers. The following para- beginning of the symptoms) occurring outside medi- meters were determined, based on the recommen- cal facilities were attested by contacted persons who dations of the American Society of Echocardiogra- directly witnessed the events. phy:9 left ventricular end-diastolic (LVID) and end- Follow-up was undertaken every 2 weeks until systolic (LVIS) internal diameters and left ventricu- blood pressure control and subsequently at a 2- lar end-diastolic posterior wall (PWTd) and inter- month interval, unless otherwise necessary. The ventricular septal thickness (IVSTd) and end-sys- ending of study was settled to November 1996 to tolic posterior wall thickness (PWTs). Left ensure all enrolled patients had a minimum 5-year ventricular mass was calculated based on the follow- follow-up. ing formula, normalised by body surface area to 10,11 obtain left ventricular mass index : Statistical analysis 2 = + + 3 LVMI (g/m ) 1.04 (PWTd IVSTd LVID) Quantitative variables are reported as means ± stan- − (LVID)3/BSA. dard deviation and qualitative variables as percent- ages. Clinical baseline characteristics of patients Left ventricular fractional shortening (LVFS) was separated as survivor and non-survivor groups were 12 calculated as follows : compared using two-tailed unpaired t-test and chi- 17 LVFS (%) = [(LVID − LVIS)/LVID] × 100. square test when appropriate, considering the P- value 0.05 as statistically significant. Left ventricular end-systolic meridional wall stress Survival curves were estimated by the Kaplan– (LVESS) was calculated based on a previously vali- Meier product-limit method.18 The log-rank test was dated non-invasive method,13,14 in which cuff used for statistical comparisons between the sur- systolic blood pressure (SBP), obtained during left vival probability curves of each of the following ventricular tracing recordings, is employed as corre- qualitative variables: gender, the presence of electro- sponding to left ventricular peak-systolic pressure: cardiographic left ventricular hypertrophy and LVESS (103/dyn/cm−2) = 0.334 × SBP strain and the presence of frequent or complex ven- tricular arrhythmias as defined above or the pres- × LVIS/PWTs × (1 + PWTs/LVIS). ence of either one of the three criteria contemplated separately. In addition, the log rank tests for the Ambulatory ECG monitoring association of survival times with each continuous variable such as age, systolic and diastolic blood Immediately after the echocardiographic study a 24- pressure, left ventricular mass index, left ventricular h ECG monitoring was undertaken during each fractional
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