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Left ventricular hypertrophy or thickening of the heart muscle is a response to excess stress or workload. It can be associated with hypertension or heart valve disease. In some unusual instances, it can be related to other disease processes such as infiltrative diseases or genetic disorders. According to your history, it seems that the most likely explanation could be hypertension. The use of medications such as ACE inhibitors, for example, Ramipril, can help to control both hypertension and the thickening – hypertrophy. Other agents that can help reduce blood pressure are calcium channel blockers, diuretics, and Angiotensin receptor blockers. Your physicians can direct the best possible combination. The goal would be to maintain the average systolic blood pressure less than 140 mmHg, the lower the better (eg 130 mmHg). Low sodium intake and active lifestyle are fundamental. There is no solid evidence for the role of EECP. Journal Article Kostas A. Gatzoulis, 1 University and State Cardiology Divisions, Hippokration General Hospital , Athens , Greece Fragogianni 34, GR-156 69 Papagos-Athens , Greece Search for other works by this author on: Gregory P. Vyssoulis,1 University and State Cardiology Divisions, Hippokration General Hospital , Athens , Greece Search for other works by this author on: Theodoros Apostolopoulos,1 University and State Cardiology Divisions, Hippokration General Hospital , Athens , Greece Search for other works by this author on: Polychronis Delaveris,1 University and State Cardiology Divisions, Hippokration General Hospital , Athens , Greece Search for other works by this author on: Artemisia Theopistou,1 University and State Cardiology Divisions, Hippokration General Hospital , Athens , Greece Search for other works by this author on: John H. Gialafos,1 University and State Cardiology Divisions, Hippokration General Hospital , Athens , Greece Search for other works by this author on: Pavlos K. Toutouzas1 University and State Cardiology Divisions, Hippokration General Hospital , Athens , Greece Search for other works by this author on:
Close Navbar Search Filter Microsite Search Term Search AbstractLeft 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. The prevalence of essential hypertension in the general population is high.1 The introduction of a variety of antihypertensive agents has significantly decreased the incidence of major complications from target organ damage when these agents are employed at early stages of the disease.2 The cardiac manifestations of systemic hypertension include left ventricular hypertrophy (LVH) at early stages and dilatation with left ventricular dysfunction at late decompensated stages. Both have been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death.3 The latter has been observed in patients in whom the electrocardiographic presence of LVH was also associated with an increased incidence of congestive heart failure, coronary heart disease, acute myocardial infarction, and a total 12-year mortality of 59%.3, 4, 5 However, the identification of hypertensive patients with electrocardiographic evidence of LVH is an uncommon event today.6 On the contrary, the presence of LVH by echocardiographic examination is reported in more than half of hypertensive patients from the very early stages of the disease, at times even before the disease has manifested itself.6–9 It appears that even the echocardiographic presence of LVH is an adverse prognostic indicator.10, 11 This, in conjunction with evidence that LVH regression can be achieved with different antihypertensive drugs, makes echocardiographic detection of LVH at early stages of the disease a desirable goal.12–14 In this study we examined whether mild LVH in ambulatory asymptomatic patients with essential hypertension is associated with significant arrhythmogenic changes resulting in adverse clinical events on the long-term follow-up. Materials and methodsOne hundred consecutive hypertensive patients first seen in an ambulatory hypertension clinic comprise the study population. All patients were studied at baseline, after discontinuation of previous antihypertensive therapy for at least four half-lives. The diagnosis of hypertension was established by at least three measurements at rest and on different occasions of greater than 140/90 mm Hg. Secondary causes of hypertension as revealed by laboratory examination were excluded. None of the patients had coronary artery disease, valvular heart disease, hypertrophic or dilated cardiomyopathy, diabetes mellitus or other endocrine disease, syncope, or a history of malignant arrhythmias. Patients taking antiarrhythmic agents or with bundle branch block were excluded. A complete physical examination, M-mode, two-dimensional echocardiography, 12-lead electrocardiography, 24-h electrocardiographic recording, and signal-averaged electrocardiography were completed in all patients using standard techniques. Echocardiographic studiesM-mode and two-dimensional echocardiograms were obtained according to the criteria of the American Society of Echocardiography.15 Left ventricle mass (LVM) was calculated by the equation LVM = (interventricular septum thickness + posterior wall thickness + end-diastolic diameter)3 − end-diastolic volume × 1.04, as reported.16 Left ventricle mass index was calculated by the ratio of LVM to body surface area. Left ventricular hypertrophy was defined as LVM index (LVMI) > 130 g/m2. 12-Lead electrocardiography (ECG)Standard 12-lead ECG were recorded on a three-channel Marquette recorder with the patient in the supine position. The following parameters were analyzed: sum of R-wave amplitude in lead I and S-wave amplitude in lead III (R1S3); R-wave amplitude in leads avL, avF, V5, or V6; S-wave amplitude in lead V1; sum of S-wave amplitude in lead V1 and R-wave amplitude in leads V5 or V6; presence of left atrial enlargement (LAE) or left axis deviation (LAD); QRS duration; intrinsicoid duration; Estes score; and voltage criteria for LVH. 24-h electrocardiographic recordingAmbulatory ECG recordings using two-channel Oxford Medilog II TM MR45 (Oxford Medical Instruments, Abington, Oxon, UK) recorders were obtained. Modified V1 and V5 leads were recorded. Patients were instructed to use the event button of the recorder whenever they felt any precordial distress. The following parameters were analyzed: mean heart rate, maximal heart rate, minimal heart rate, number of premature ventricular contractions per hour (PVC/h), occurrence of multiform PVC/24 h, occurrence of R-on-T phenomenon, number of ventricular couplets/24 h, number of nonsustained or sustained VT episodes/24 h, where sustained VT was defined as VT episodes of more than 30 s in duration. Signal-averaged electrocardiographySignal-averaging (40- to 250-Hz filtering) was obtained with a Corazonix predictor according to a previously described technique.17 Up to 600 cardiac cycles were averaged to reduce the noise level below 0.5 μV. The following parameters were calculated: filtered QRS duration (Flt QRS), low-amplitude signal duration (LAS), root mean square voltage of the last 40 ms of the filtered QRS complex (RMS-40), and presence of late potentials (conventional European Society of Cardiology/American Heart Association/American College of Cardiology criteria were used). Laboratory examinationsSerum lipid determinations were done on fresh plasma samples collected after 12 h of fasting. Total and high-density lipoprotein (HDL) cholesterol were measured by the enzymatic colorimetric and the phosphotungstate method.18 Plasma renin activity was measured in the morning, after 30 min of rest in the supine position in a quiet room, using the Clinical Assays plasma renin activity radioimmunoassay kit.19 Standard laboratory examinations were done in all patients, to exclude secondary forms of hypertension or the coexistence of other systemic diseases. Hypertensive patients were treated with either a calcium channel blocker (amlodipine) or an angiotensin converting enzyme inhibitor (lisinopril) to achieve blood pressure values < 140/90 mm Hg at rest, or a fall of > 10 mm Hg in diastolic blood pressure. Based on echocardiographic criteria for LVH, the study population was divided into two groups: Group 1 (G1) comprised 35 hypertensive patients without LVH (mean left ventricular mass index [LVMI], 112 ± 22 g/m2) and Group 2 (G2) of 65 hypertensive patients with LVH (mean LVMI; 156 ± 24 g/m2). Clinical follow-upAll patients were seen at the Hypertension Clinic at 3-month intervals. Complaints such as severe palpitations, presyncope or syncope attacks, and hospitalizations for sustained ventricular arrhythmias were recorded. StatisticsResults are expressed as mean values ± 1 standard deviation. Comparison of mean values between the groups with and without LVH was done using the unpaired Student’s t test and percentages were compared with the χ2 test. A P value less than .05 was considered significant. ResultsPatient’s clinical characteristics are presented in Table 1. Hypertensive patients with echocardiographic criteria for LVH were older, with higher systolic blood pressure at rest, and larger body mass index and body surface area. The 12-lead electrocardiographic data are shown in Table 2. None of the electrocardiographic variables examined differed between the two groups. Although the Estes score was higher among the hypertensive patients with echocardiographic LVH, the difference did not reach statistical significance and the mean value observed (1.3 ± 1.8) was far from fulfilling the electrocardiographic criteria for left ventricular hypertrophy. The QRS as well as the intrinsicoid duration were similar among the two groups. The detection of either left atrial enlargement or left axis deviation was uncommon in either group. Similarly, voltage criteria for LVH were uncommonly met in either group. Table 1. Patients’ Clinical Characteristics
G1, patients without left ventricular hypertrophy; G2, patients with left ventricular hypertrophy; SBP, systolic blood pressure at rest; DBP, diastolic blood pressure at rest; BMI, body mass index; BSA, body surface area; NS, not significant. Table 1. Patients’ Clinical Characteristics
G1, patients without left ventricular hypertrophy; G2, patients with left ventricular hypertrophy; SBP, systolic blood pressure at rest; DBP, diastolic blood pressure at rest; BMI, body mass index; BSA, body surface area; NS, not significant. Table 2. 12-Lead electrocardiographic data
G1, patients without LVH; G2, patients with LVH; RAVL, R-wave amplitude in lead aVL; RAVF, R-wave amplitude in lead aVF; R1S3, sum of R- and S-wave amplitudes in leads I and III, respectively; SV1, S-wave amplitude in lead V1; RV5,6; tallest R-wave amplitude in either lead V5 or V6; QRS, QRS duration; LAE, presence of left atrial enlargement; LAD, presence of left axis deviation; Intrins, intrinsicoid duration; Estes SC, Estes score; voltage/LVH, presence of voltage criteria for LVH; LVH, left ventricular hypertrophy; NS, not significant. Table 2. 12-Lead electrocardiographic data
G1, patients without LVH; G2, patients with LVH; RAVL, R-wave amplitude in lead aVL; RAVF, R-wave amplitude in lead aVF; R1S3, sum of R- and S-wave amplitudes in leads I and III, respectively; SV1, S-wave amplitude in lead V1; RV5,6; tallest R-wave amplitude in either lead V5 or V6; QRS, QRS duration; LAE, presence of left atrial enlargement; LAD, presence of left axis deviation; Intrins, intrinsicoid duration; Estes SC, Estes score; voltage/LVH, presence of voltage criteria for LVH; LVH, left ventricular hypertrophy; NS, not significant. The results of the 24-h electrocardiographic recordings in the two patient groups are presented in Table 3. Mean heart rate as well as the maximal and minimal heart rate values observed during the 24-h recording period were similar in both hypertensive groups. The number of premature ventricular contractions per hour of recording was low (< 10 PVC/h) and was not affected by the presence of echocardiographic LVH. The vast majority of the premature ventricular contractions were uniform. A similar minority of hypertensive patients in both groups had multiformed premature ventricular contractions (7.4% in G1v 7.8% in G2 patients). R-on-T phenomenon was documented in only one hypertensive patient with echocardiographic evidence for LVH. The occurrence of ventricular couplets was a rare event during the recording period in both hypertensive patient groups. Potentially malignant or malignant ventricular arrhythmias in the form of unsustained or sustained ventricular tachycardia were not detected in any of the 100 hypertensive patients studied. Table 3. 24-H electrocardiographic data
G1, patients without left ventricular hypertrophy; G2, patients with left ventricular hypertrophy; bpm, beats per minute; Mean HR, mean heart rate; Max HR, maximal heart rate; Min HR, minimal heart rate; PVC/h, number of premature ventricular contractions per hour; multiform PVC (%), percentage of patients with more than one morphology of premature ventricular contractions during the 24-h recording period; R-on-T (%), percentage of patients with early (R-on-T phenomenon) premature ventricular contractions; Vcoup/24 h; number of ventricular couplets during the 24-h recording period; VTruns/24 h, number of ventricular tachycardia episodes observed during the 24-h recording period; NS, not significant. Table 3. 24-H electrocardiographic data
G1, patients without left ventricular hypertrophy; G2, patients with left ventricular hypertrophy; bpm, beats per minute; Mean HR, mean heart rate; Max HR, maximal heart rate; Min HR, minimal heart rate; PVC/h, number of premature ventricular contractions per hour; multiform PVC (%), percentage of patients with more than one morphology of premature ventricular contractions during the 24-h recording period; R-on-T (%), percentage of patients with early (R-on-T phenomenon) premature ventricular contractions; Vcoup/24 h; number of ventricular couplets during the 24-h recording period; VTruns/24 h, number of ventricular tachycardia episodes observed during the 24-h recording period; NS, not significant. The results of the signal-averaged electrocardiography are summarized in Table 4. A satisfactory noise level was achieved in both groups studied (0.38 ± 0.2 μV in G1v 0.42 ± 0.2 μV in G2, P = NS). Although there was a minimal trend for the filtered QRS duration and the low-amplitude signal duration to be longer in the hypertensive group with echocardiographic LVH, there was no statistically detected difference between the two groups. Similarly, the root mean square voltage of the last 40 ms of the filtered QRS complex was not different between the two groups. Using the ESC/AHA/ACC Task Force criteria for the presence of late potentials, at least one abnormal value was detected in a similar proportion of hypertensives (35.4% in G1 patients v 33.3% in G2 patients). Even when more stringent signal averaged electrocardiogram (SAECG) criteria, such as the presence of two abnormal parameters, were applied, no difference was detected (16.1% in G1v 15.8% in G2 patients). All three parameters were abnormal in a similar minority of both groups (3.2% in G1v 3.5% in G2 patients). Table 4. Signal-averaged electrocardiographic data
G1, patients without left ventricular hypertrophy; G2, patients with left ventricular hypertrophy; FQRS, filtered QRS duration; LAS, low-amplitude signal duration; RMS, root mean square of the last 40 ms of the filtered QRS complex; LPs, late potentials; NS, not significant. Table 4. Signal-averaged electrocardiographic data
G1, patients without left ventricular hypertrophy; G2, patients with left ventricular hypertrophy; FQRS, filtered QRS duration; LAS, low-amplitude signal duration; RMS, root mean square of the last 40 ms of the filtered QRS complex; LPs, late potentials; NS, not significant. Patients in both groups had reduced LV wall thickness and LV mass after 6 months of antihypertensive treatment (Table 5). LV mass index was reduced more in patients with baseline LVH (−12% v −7%, P < .0001). Table 5. Patient data after 6 months’ antihypertensive treatment
* P < 0.05 for within-group differences † P < 0.05 for between-group differences. LV, left ventricular; G1, patients with LV hypertrophy; G2, patients without LV hypertrophy; EDD, LV end-diastolic diameter; IVSd, LV interventricular septum diastolic thickness; PWd, LV posterior wall diastolic thickness; LVMI, LV mass index; LVEF, LV ejection fraction; PRA, plasma renin activity; HDL, high-density lipoprotein. Table 5. Patient data after 6 months’ antihypertensive treatment
* P < 0.05 for within-group differences † P < 0.05 for between-group differences. LV, left ventricular; G1, patients with LV hypertrophy; G2, patients without LV hypertrophy; EDD, LV end-diastolic diameter; IVSd, LV interventricular septum diastolic thickness; PWd, LV posterior wall diastolic thickness; LVMI, LV mass index; LVEF, LV ejection fraction; PRA, plasma renin activity; HDL, high-density lipoprotein. Plasma renin activity and serum lipids had similar values in both groups at baseline, and did not change significantly posttreatment (P = NS). During the 3 ± 1 years of follow-up, no arrhythmic events were detected in either group. Specifically, none of the patients complained of severe palpitations, presyncope, or syncope. There was no hospitalization for sustained ventricular arrhythmias and all patients remain alive. DiscussionThis prospective study examined 100 asymptomatic ambulatory hypertensive patients of an ambulatory hypertension clinic with a noninvasive ventricular arrhythmia work-up. None of the patients had a known history of cardiac disorder, syncope, or life-threatening arrhythmias and thus the arrhythmia work-up findings could safely be attributed to the systemic hypertension alone. Although electrocardiographic criteria for LVH were uncommonly met in our study group (6.5%), such echocardiographic criteria were present in 65 patients (65%). This is in accordance with previous studies showing the high sensitivity of the echocardiogram for the detection of LVH among hypertensive patients.6, 7, 8, 9 The hypertensive patients with echocardiographic evidence for LVH were older with higher systolic blood pressure at rest and a larger body mass index. However, their contractility indices did not differ from their counterparts without LVH. The degree of LVH as expressed by the LVMI could be characterized as mild to moderate.20 Despite the presence of mild LVH, the examined 12-lead electrocardiographic variables were not significantly affected when compared with the hypertensive patients without LVH. Although the Estes scores reached a higher value in the LVH group (1.3 ± 1.8 v 0.8 ± 1.6), the difference was not significant and the observed score value was far from that proposed for the ECG presence of LVH.21 Potentially malignant or malignant ventricular arrhythmias, namely unsustained or sustained ventricular tachyarrhythmias, were not observed in either hypertensive patient group during the 24-h recording period.22 Such life-threatening ventricular arrhythmias have been documented in hypertensive patients with severe LVH (LVMI > 200 g/m2) or depressed left ventricular function and thus are manifestations of advanced hypertensive heart disease if not of a subpopulation of hypertensive patients not yet well examined.23, 24, 25 Complex forms of ventricular ectopic activity were also rarely seen in the hypertensive groups studied. Indeed, R-on-T phenomenon was seen in only one patient, ventricular couplets were rare, and multiformed premature ventricular contractions were present in less than 8% of both patient groups. Similarly, the incidence of simpler forms of ventricular ectopy, such as premature ventricular contractions, was similar and low in both groups (6.8 ± 2.1 v 6.0 ± 1.9 PVC/h, P = NS). Thus, contrary to previous studies, the presence of mild LVH was not associated with an increased incidence of either simple or complex forms of ventricular ectopy.26, 27 This discrepancy may be due to different patient populations studied, the retrospective nature of many previous studies, the age and severity of LVH, or to the well-known variability of Holter findings. We believe our hypertensive patients studied reflect the average hypertensive patient without other concomitant cardiac disorders presenting in an outpatient clinic on a daily basis. Similarities to our results among hypertensive patients with mild forms of LVH have been reported by others.7, 28 The signal-averaged electrocardiogram indices were also not affected by the presence of mild LVH. Similarly, the incidence of late potentials using different criteria of positivity was not different in both groups examined. When defining late potentials by the presence of at least one abnormal SAECG value, these markers of delayed and nonhomogeneous ventricular activation were commonly met among our hypertensives regardless of the presence of mild LVH on echocardiography. However, only three of the 100 patients examined (two patients with LVH) had all three SAECG parameters abnormal. These observations are in agreement with previous reports.7, 29, 30 A much lower incidence of late potentials among hypertensives with preserved left ventricular systolic function has been reported by others.24, 31, 32 It is interesting that among hypertensives with advanced degrees of LVH, left ventricular dysfunction, and a history of malignant ventricular arrhythmias, all three SAECG parameters defining late potentials are commonly abnormal.24 In this hypertensive patient cohort examined, we found the presence of mild echocardiographically detected LVH not to be associated with adverse clinical events during the 3-year follow-up. This could be due to the application of appropriate antihypertensive treatment resulting in LVH regression and adequate blood pressure control. Nevertheless, even at baseline, when the two groups were compared using a variety of noninvasive arrhythmia indices, there were no additional significant arrhythmogenic changes induced by the presence of mild LVH. It is likely that such changes occur with advanced forms of LVH or in hypertensive patients with associated cardiac disorders or left ventricular dysfunction. Thus it is highly desirable to initiate appropriate antihypertensive therapy at early stages when mild LVH has not yet resulted in significant arrhythmia substrate changes. It would be expected that regression of LVH by such therapy will prevent serious future arrhythmia events. LimitationsThe degree of left ventricular hypertrophy in this hypertensive study population was mild. Thus extrapolations for hypertensive patients with more advanced forms of left ventricular hypertrophy are not valid. Furthermore, elderly hypertensives were rather few among our patient population. It would be interesting to explore the arrhythmogenic effect of old age and severe left ventricular hypertrophy in a future study. ConclusionIn this study we did not find any correlation between echocardiographic evidence for mild LVH and worrisome arrhythmologic abberations among 100 ambulatory patients with essential hypertension. Although the incidence of simple forms of ventricular ectopy and late potentials was not unremarkable in both hypertensive groups examined, the long-term clinical follow-up was free of any significant arrhythmic clinical events. References1. National High Blood Pressure Education Program : The fifth report of the joint national committee on detection, evaluation and treatment of high blood pressure . National Heart, Lung and Blood Institute , 1993 : NIH Publication 93-1088 . 2. IPPPSH Collaborative Group Cardiovascular risk and risk factors in a randomized trial of treatment based on the beta-blocker oxprenolol: the International Prospective Primary Prevention Study in Hypertension (IPPSH) . J Hypertension 1995 ; 3 : 379 . 3., , : Left ventricular hypertrophy by electrocardiogram: prevalence, incidence and mortality in the Framingham Study . Ann Intern Med 1969 ; 71 : 89 – 105 . 4., , , , : Role of blood pressure in the development of congestive heart failure: the Framingham Study . N Engl J Med 1972 ; 287 : 781 – 787 . 5., , , : Electrocardiographic left ventricular hypertrophy and risk of coronary heart disease. The Framingham study . Ann Intern Med 1970 ; 72 : 813 – 822 . 6.: : Left ventricular hypertrophy, arrhythmias and sudden death in systemic hypertension . Am J Cardiol 1987 ; 60 : 131 – 181 . 7., , , , , : Study of late potentials and ventricular arrhythmias in hypertensive patients with normal electrocardiograms . PACE 1994 ; 17 : 577 – 584 . 8., , , , , , : The prevalence and correlates of echocardiographic left ventricular hypertrophy among employed patients with uncomplicated hypertension . J Am Coll Cardiol 1986 ; 7 : 639 – 650 . 9., , , , : Left ventricular mass as a predictor of development of hypertension . Am J Hypertens 1991 ; 4 : 6035 – 6075 . 10., , , , : Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study . N Engl J Med 1990 ; 322 : 1561 – 1566 . 11., , , , : Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension . Ann Intern Med 1991 ; 114 : 342 – 345 . 12., , : Reversal of left ventricular hypertrophy in hypertensive patients. A metanalysis of 109 treatment studies . Am J Hypertension 1992 ; 5 : 95 – 100 . 13., , , : Cardiovascular effects of verapamil in patients with essential hypertension . Circulation 1987 ; 75 : 1030 – 1036 . 14., , , : Changes in ventricular septal thickness during diuretic therapy . Clin Pharmacol Ther 1982 ; 32 : 283 – 288 . 15., , , : Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements . Circulation 1978 ; 58 : 1072 – 1083 . 16., , , , : Significance of blood pressure levels achieved with felodipine anti-hypertensive treatment on cardiovascular structure and function changes . J Hum Hyperten 1998 ; 12 : 427 – 432 . 17., , , , , , : Time domain analysis of the signal averaged electrocardiogram in patients with a conduction defect or a bundle branch block . Eur Heart J 1995 ; 16 : 1912 – 1919 . 18., , , , , : Differentiation of β-blocker effects on serum lipids and apolipoproteins in hypertensive patients with normolipidaemic or dislipidaemic profiles . Eur Heart J 1992 ; 13 : 1506 – 1513 . 19., , , , : Ambulatory blood pressure changes in the menstrual cycle of hypertensive women. Significance of plasma renin activity values . Am J Hypertens 1993 ; 6 : 654 – 659 . 20., : Echocardiographic determination of left ventricular mass in man . Circulation 1977 ; 55 : 613 – 618 . 21., : A point score system for the ECG diagnosis of left ventricular hypertrophy . Am Heart J 1968 ; 75 : 752 – 758 . 22.: : Identification of patients at high risk for sudden cardiac death . Am J Cardiol 1984 ; 54 : 3D . 23., , , : Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy . N Engl J Med 1987 ; 317 : 787 – 792 . 24., , , , : Electrophysiological and therapeutic implications of cardiac arrhythmias in hypertension . Eur Heart J 1992 ; 13 : ( suppl D ): 70 – 81 . 25., , , : Usefulness of echocardiographic LVH, ventricular tachycardia and complex ventricular arrhythmias in predicting ventricular fibrillation or sudden cardiac death in elderly patients . Am J Cardiol 1988 ; 62 : 1124 – 1125 . 26., , , , : Hypertension and sudden death: increased ventricular ectopic activity in left ventricular hypertrophy . Am J Med 1984 ; 77 : 18 – 22 . 27., : Hypertension, left ventricular hypertrophy, ventricular arrhythmias and sudden death . Eur Heart J 1992 ; 13 : ( suppl D ): 66 – 69 . 28., , , : Hypertensive concentric left ventricular hypertrophy when is ventricular ectopic activity increased? . South Med J 1988 ; 81 : 696 – 700 . 29., , , , , : Late potentials in patients with hypertension . Arch Mal Coeur Vaiss 1990 ; 83 : 1165 – 1168 . 30., , , , , : Prevalence of late ventricular potentials in hypertensive patients . J Cardiovasc Pharmacol 1991 ; 17 : ( suppl 2 ): S146 – S147 . 31., , , : Ventricular arrhythmias in hypertensive heart disease with and without heart failure . J Cardiovasc Pharm 1987 ; 10 : ( suppl 6 ): 119 – 128 . 32., , , , , : Significance of ventricular arrhythmias in systemic hypertension with left ventricular hypertrophy . Am J Cardiol 1992 ; 69 : 913 – 917 . © 2000 by the American Journal of Hypertension, Ltd. American Journal of Hypertension, Ltd. © 2000 by the American Journal of Hypertension, Ltd. Topic:
Is mild concentric left ventricular hypertrophy serious?It's important to treat the causes of LVH early because it can lead to severe problems such as heart failure, sudden cardiac arrest and ischemic stroke.
How is mild concentric LVH treated?Treatment. Angiotensin-converting enzyme inhibitors. Also called ACE inhibitors, these medications widen blood vessels to lower blood pressure. ... . Angiotensin II receptor blockers. ... . Beta blockers. ... . Calcium channel blockers. ... . Water pills, also called diuretics.. Can mild concentric left ventricular hypertrophy be reversed?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.
What is the treatment of left ventricular hypertrophy?Treating high blood pressure can help reduce left ventricular hypertrophy symptoms and may even reverse it. Narrowing of the aortic valve. The aortic valve is between the lower left heart chamber and the body's main artery, called the aorta. Narrowing of the valve is called aortic stenosis.
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What does mild concentric left ventricular hypertrophy mean
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