Regression Of Electrocardiographic Left Ventricular Hypertrophy Research Articles

Regression of Electrocardiographic Left Ventricular Hypertrophy After Transcatheter Aortic Valve Implantation for Aortic Stenosis.

The changes in electrocardiographic left ventricular hypertrophy (ECG-LVH) after transcatheter aortic valve implantation (TAVI) are not fully elucidated.Methods and Results:The study group included 64 patients who underwent TAVI for aortic stenosis. Their 12-lead ECGs before and at 2 days and 1, 6 and 12 months after TAVI were analyzed, and ECG-LVH was evaluated using various definitions. Values and prevalence of each ECG-LVH parameter significantly decreased between 1 and 6 months after TAVI. Values of ECG-LVH parameters decreased especially in patients with ECG-LVH at baseline. Regression of ECG-LVH was observed between 1 and 6 months after TAVI.

Regression of Electrocardiographic Signs of Left Ventricular Hypertrophy by Combined Treatment With Thiazide Diuretic and Angiotensin-II Receptor Blocker.

In hypertensive patients, left ventricular hypertrophy (LVH) may persist despite satisfactory blood pressure (BP) control. The efficacy of thiazide diuretics in Western countries has been reported, but whether this applies to hypertensive Japanese patients is uncertain. METHODS AND RESULTS: We randomly assigned 94 patients whose BP was poorly controlled with usual doses of angiotensin-II receptor blockers (ARB), to losartan/hydrochlorothiazide (HCTZ) fixed-dose combination vs. maximum doses of ARB. After 6 months follow-up, decrease in BP, regression of electrocardiographic LVH, and changes in laboratory measurements were examined. Although a similar decrease in BP was observed in both groups, the decrease in LV Sokolow-Lyon voltage, from 34.4±9.2 to 29.4±8.8 mm in the losartan/HCTZ vs. from 29.9±10.2 to 29.1±8.4 mm in the ARB group (P=0.0003), and the decrease in serum B-type natriuretic peptide (BNP) level, from 30.1±28.5 to 26.8±28.0 pg/ml vs. from 23.7±14.8 to 29.8±29.3 pg/ml (P=0.045) were greater in the losartan/HCTZ group. By single variable logistic regression analysis, ∆BNP (P=0.012) and treatment with losartan/HCTZ (P<0.0001) correlated with the regression of LVH. By multiple variable logistic regression analysis, both ∆BNP (P=0.035) and treatment with losartan/HCTZ (P=0.0003) remained significant. No major adverse effects were observed. Greater regression of LVH was safely achieved with losartan/HCTZ in patients whose BP was poorly controlled with an ARB.

Regression of ECG-LVH is Associated with Lower Risk of New-Onset Heart Failure and Mortality in Patients with Isolated Systolic Hypertension; The LIFE Study

Hypertension and electrocardiographic left ventricular hypertrophy (ECG-LVH) are strong predictors of heart failure (HF). It is unclear whether regression of ECG-LVH during treatment predicts less new-onset HF in patients with isolated systolic hypertension (ISH). A total of 9,027 patients with hypertension and ECG-LVH and without a history of HF were randomized to losartan- or atenolol-based treatment in the Losartan Intervention For Endpoint reduction in hypertension study. Incident HF and the combined endpoint of HF and death were evaluated in 1,280 ISH patients and as compared with 7,747 patients with systolic-diastolic hypertension or isolated diastolic hypertension (non-ISH) during mean 4.8 ± 0.9 years follow-up. New-onset HF and HF or death occurred in 57 (4.5%) and 179 (14.0%) ISH patients and 220 (2.8%) and 787 (10.2%) non-ISH patients. In Cox regression analyses adjusting for treatment and HF risk factors, time-varying Cornell product was associated with lower risk of new-onset HF in ISH (adjusted hazard ratio (HR) 0.79, 95% confidence interval (CI) 0.67-0.94, P = 0.008, per 1,050 mm × ms (1 SD) lower Cornell product) and in non-ISH (adjusted HR 0.67, 95% CI 0.61-0.72, P < 0.001, per SD lower Cornell product). In parallel analyses, time-varying Cornell product was associated with lower risk of new-onset HF or death in ISH and non-ISH (adjusted HR 0.83, 95% CI 0.75-0.93, P = 0.001 and 0.82, 95% CI 0.77-0.87, P < 0.001, per SD lower Cornell product). Regression of time-varying Cornell product was associated with similar reductions in risk of new-onset HF and the combined endpoint of HF or death in ISH and non-ISH patients.

Greater Regression of Electrocardiographic Left Ventricular Hypertrophy During Hydrochlorothiazide Therapy in Hypertensive Patients

Treatment of hypertensive patients with a losartan-based regimen was associated with greater regression of electrocardiographic (ECG) left ventricular hypertrophy (LVH) than atenolol-based therapy in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, independent of blood pressure (BP) changes. However, whether concomitant hydrochlorothiazide (HCTZ) therapy in >70% of LIFE patients was associated with greater regression of LVH independent of BP changes and whether this effect differed between treatment arms has not been examined. Changes in Cornell product and Sokolow-Lyon voltage LVH were assessed in 9,193 hypertensive patients randomly assigned to treatment with losartan or atenolol, with additional HCTZ therapy added as necessary to achieve target BP goal per study protocol. After controlling for baseline and change in systolic and diastolic pressure, age, sex, race, prior antihypertensive treatment, baseline and year-4 body mass index and baseline LVH by either Cornell product or Sokolow-Lyon voltage, at year-4 follow-up HCTZ therapy was associated with greater regression of Cornell product LVH (-244 +/- 788 vs. -172 +/- 771 mm.msec, P < 0.05) and Sokolow-Lyon voltage (-4.2 +/- 6.7 vs. -3.0 +/- 7.0 mm, P < 0.001) and this effect was significantly greater in patients on losartan (-341 +/- 743 vs. -189 +/- 775 mm.msec and -5.2 +/- 6.6 vs. -3.3 +/- 6.6 mm) than in patients on atenolol (-142 +/- 822 vs. -158 +/- 765 mm.msec and -3.1 +/- 6.6 vs. -2.7 +/- 7.4 mm; both P < 0.001 for interaction of HCTZ with losartan vs. atenolol therapy). HCTZ use was associated with greater regression of ECG LVH and this effect was greater in patients on losartan- than atenolol-based therapy, independent of baseline severity of ECG LVH and hypertension and changes in BP.

Incidence of heart failure in relation to QRS duration during antihypertensive therapy: the LIFE study

Prolonged QRS duration (QRS) has been associated with left ventricular dyssynchrony and dysfunction and with the development of heart failure. However, whether persistence or development of increased QRS over time is associated with an increased incidence of heart failure in hypertensive patients, independent of blood pressure lowering and regression of electrocardiographic left ventricular hypertrophy (LVH) has not been examined. The relation of QRS over time to incident heart failure was examined in 8945 hypertensive patients without history of heart failure who were randomly assigned to losartan-based or atenolol-based treatment. During 4.7 +/- 1.1 years follow-up, heart failure hospitalization occurred in 282 patients (3.2%): in 157 with in-treatment QRS less than 110 ms (4.6 per 1000 patient-years) and in 125 with persistence or development of QRS 110 ms or more (13.4 per 1000 patient-years). In univariate Cox analyses in which QRS during the study was entered as a time-varying covariate, in-treatment persistence or development of a QRS 110 ms or more was associated with a 153% increased risk of developing heart failure [hazard ratio 2.53, 95% confidence interval (CI) 2.00-3.20]. After adjusting for treatment, baseline risk factors for heart failure, incident myocardial infarction and for baseline and in-treatment electrocardiographic LVH and blood pressure, persistence or development of a QRS 110 ms or more remained associated with a 102% increased risk of new-onset heart failure (hazard ratio 2.02, 95% CI 1.49-2.74). Persistence or development of a prolonged QRS during antihypertensive therapy is associated with an increased likelihood of new-onset heart failure, independent of blood pressure lowering, treatment modality and regression of electrocardiographic LVH in patients with essential hypertension. These findings suggest that serial assessment of QRS over time can be used to track the risk of heart failure in hypertensive patients.

Electrocardiographic left ventricular hypertrophy regression induced by an angiotensin receptor blocker-based regimen in hypertensive patients with diabetes: data from the SARA study

This study examined the influence of diabetes on left ventricular hypertrophy (LVH) detected by different electrocardiographic (ECG) criteria and its changes induced by a 12-month candesartan-based regimen. The patients were treated for a 12-month period with a candesartan-based regimen (8/16 mg + hydrochlorothiazide12.5 mg + additional drugs to target blood pressure < 140/90 mmHg [< 130/80 in diabetics]). Cornell voltage index (CorV), Cornell product (CorP), Sokolow-Lyon voltage index (SokV), and Sokolow-Lyon product (SokP) were calculated. In total 276 patients were included, 51 with diabetes. At study end, blood pressure was reduced 19.0+/-9.2/7.3+/-3.4 mmHg in diabetic patients and 18.8+/-9.1/8.0+/-3.2 mmHg in non-diabetic subjects (both p<0.01 vs. baseline; p=0.85 between groups).At baseline, 37.5% of diabetic and 26.4% of non-diabetic patients fulfilled criteria of ECG-LVH by CorP (p=0.02), 25.7% and 23.2%, respectively, by SokP (p=0.18), 11.8% and 13.7% by CorV (p=0.16), and 14.3% and 11.6% by SokV (p=0.10).At study end, the prevalence of ECG-LVH was reduced to 25.1% (relative risk reduction [RRR] 33.3%, p=0.001) and 18.2% (RRR 29.2%, p=0.001) by CorP and SokP, in diabetic patients, respectively. In non-diabetic patients, only the CorP criterion showed a significant decrease (RRR 18.9%, p=0.01). No significant changes were observed by other criteria.The RRR of ECG-LVH with treatment was significantly higher in diabetics according to CorP and SokP criteria. The prevalence of ECG-LVH detected by CorP was higher in diabetics. Diabetics achieved higher reductions in ECG-LVH prevalence than non-diabetics with a candesartan-based regimen.

Serial evaluation of electrocardiographic left ventricular hypertrophy for prediction of risk in hypertensive patients

Background Although the presence and severity of electrocardiographic (ECG) left ventricular hypertrophy (LVH) have been associated with an increased risk of cardiovascular (CV) morbidity and mortality, the relationship of regression of ECG LVH during antihypertensive therapy to CV risk has only recently been examined. Methods Electrocardiographic LVH was evaluated over time in 9193 hypertensive patients enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension study. Patients were treated with losartan- or atenolol-based regimens and followed with serial ECGs at 6 months and then yearly until death or study end. Electrocardiographic LVH was measured using gender-adjusted Cornell product (RaVL + SV3 [+6 mm in women]) ⁎ QRS duration) and Sokolow-Lyon voltage (SV1 + RV5/6). Results After mean (SD) follow-up of 4.8 (0.9) years, the Losartan Intervention for Endpoint Reduction in Hypertension study composite end point of CV death, nonfatal myocardial infarction, or stroke occurred in 1096 patients. In Cox regression models controlling for treatment type, baseline Framingham risk score, baseline, and in-treatment blood pressure and for severity of baseline ECG LVH by Cornell product and Sokolow-Lyon voltage, lower in-treatment ECG LVH by Cornell product and Sokolow-Lyon voltage were associated with 14% and 17% lower rates, respectively, of the composite CV end point: adjusted hazard ratios (HRs) of 0.86 (95% confidence interval [CI], 0.82-0.90; P < .001) for every 1050 mm · ms (1 SD) decrease in Cornell product and 0.83 (95% CI, 0.78-0.88; P < .001) for every 10.5 mm (1 SD) decrease in Sokolow-Lyon voltage. In parallel analyses, lower Cornell product and Sokolow- Lyon voltage were each independently associated with lower risks of CV mortality (HR, 0.78; 95% CI, 0.73-0.83; P < .001; HR, 0.80; 95% CI, 0.73-0.87; P < .001), of myocardial infarction (HR, 0.90; 95% CI, 0.82-0.98; P = .011; HR, 0.90; 95% CI, 0.81-1.00; P = .043), and of stroke (HR, 0.90; 95% CI, 0.84-0.96; P = .002; HR, 0.81; 95% CI, 0.75-0.89; P < .001). Regression of ECG LVH was also associated with significantly reduced risks of sudden cardiac death, new-onset atrial fibrillation, hospitalization for heart failure, and new-onset diabetes mellitus. Conclusions Regression of ECG LVH by Cornell product and/or Sokolow-Lyon voltage criteria during antihypertensive therapy is associated with lower likelihoods of CV morbidity and mortality, all-cause mortality, and new-onset diabetes, independent of blood pressure lowering and treatment modality in essential hypertension. These findings suggest that antihypertensive therapy targeted at regression or prevention of ECG LVH may improve prognosis.

Electrocardiographic Left Ventricular Hypertrophy Regression Induced by an Angiotensin Receptor Blocker‐Based Regimen in Hypertensive Patients With the Metabolic Syndrome: Data From the SARA Study

The authors assessed the effect of an angiotensin receptor blocker (candesartan)-based regimen on electrocardiographic left ventricular hypertrophy (ECG-LVH) in 276 patients with hypertension, including 141 with the metabolic syndrome (MS). Baseline blood pressure (BP) and ECG-LVH parameters did not differ in patients with and without MS. At the study's end, BP had decreased similarly in both groups. At baseline, 26.1% of patients with MS and 24.7% without MS exhibited ECG-LVH by Cornell product (CorP) criteria (P=NS); 26.8% and 17.2%, respectively, by Sokolow-Lyon product (SokP) (P=.01); 11.4%and 11.8% by Cornell voltage (CorV) (P=NS); and 12.4% and 6.5% by Sokolow-Lyon voltage (SokV) (P=.01). At the study's end, in the MS group, prevalence of ECG-LVH was reduced to 19.5% from 26.1% (P=.001), to 8.5% from 11.4% (P=.01), and to 24.4% from 26.8%(P=.03) by CorP, CorV, and SokP, respectively. In patients without MS, only the CorP criterion showed a significant decrease in ECG-LVH prevalence, declining to 20.5% (P=.01). The relative risk reduction of ECG-LVH was higher in patients with MS according to CorV and SokP criteria (P<.01).

Electrocardiographic left ventricular hypertrophy regression induced by an angiotensin receptor blocker-based regimen in daily clinical practice: the SARA study

Clinical trials have proved that angiotensin receptor blockers (ARB) are more effective than other antihypertensive agents in reducing left ventricular hypertrophy (LVH); however, information about the efficacy of ARB on LVH regression in daily medical practice is scarce. The aim of the SARA study was to investigate the effect of an ARB on electrocardiographic LVH (ECG-LVH) in a hypertensive outpatient population attending clinical practice. From 276 recruited patients with mild-to-moderate essential hypertension (245 uncontrolled, 31 newly diagnosed), 264 (age: 62.9+/-11.6 years; 51.2% women) completed the study and were valid for the analysis. The patients were treated for a 12-month period with a candesartan-based regimen [(8/16 mg+hydrochlorothiazide 12.5 mg+additional drugs to target BP<140/90 mmHg (<130/80 in diabetics)]. ECG changes were measured at a core laboratory and Cornell product (CorP), Sokolow-Lyon product (SokP) and QRS duration (QRSd) criteria were determined. At baseline, 27.4% of patients fulfilled the criteria of LVH by CorP. The proportion of patients with ECG-LVH by CorP criteria decreased to 21.1% at the end of the study, relative risk reduction (RRR) was 22.9%, P<0.001. When using SokP the percentage of ECG-LVH reduced from 24.1 to 21.7% (RRR 9.6%, P=0.1). Quantitatively, CorP was reduced by 84.4 mmxms [95% confidence interval (CI): -8.14, -160.66; P=0.03]; a greater reduction was detected in obese patients (P<0.05), diabetics (P<0.07) and patients with baseline ECG-LVH (P<0.05). In the multivariate analysis, female gender, baseline systolic blood pressure, baseline CorP and QRSd values were the main predictive factors for ECG-LVH regression. The SARA study demonstrates that a candesartan-based regimen reduces ECG-LVH in the hypertensive population attending daily in clinical practice.

Regression of Electrocardiographic Left Ventricular Hypertrophy and Decreased Incidence of New-Onset Atrial Fibrillation in Patients With Hypertension

Atrial fibrillation (AF) is associated with increased risk of mortality and cardiovascular events, particularly stroke, making prevention of new-onset AF a clinical priority. Although the presence and severity of electrocardiographic left ventricular hypertrophy (LVH) appear to predict development of AF, whether regression of electrocardiographic LVH is associated with a decreased incidence of AF is unclear. To test the hypothesis that in-treatment regression or continued absence of electrocardiographic LVH during antihypertensive therapy is associated with a decreased incidence of AF, independent of blood pressure and treatment modality. Double-blind, randomized, parallel-group study conducted in 1995-2001 among 8831 men and women with hypertension, aged 55-80 years (median, 67 years), with electrocardiographic LVH by Cornell voltage-duration product or Sokolow-Lyon voltage, with no history of AF, without AF on the baseline electrocardiogram, and enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension Study. Losartan- or atenolol-based treatment regimens, with follow-up assessments at 6 months and then yearly until death or study end. New-onset AF in relation to electrocardiographic LVH determined at baseline and subsequently. Electrocardiographic LVH was measured using sex-adjusted Cornell product criteria ({R(aVL) + S(V3) [+ 6 mm in women]} x QRS duration). After a mean (SD) follow-up of 4.7 (1.1) years, new-onset AF occurred in 290 patients with in-treatment regression or continued absence of Cornell product LVH for a rate of 14.9 per 1000 patient-years and in 411 patients with in-treatment persistence or development of LVH by Cornell product criteria for a rate of 19.0 per 1000 patient-years. In time-dependent Cox analyses adjusted for treatment effects, baseline differences in risk factors for AF, baseline and in-treatment blood pressure, and baseline severity of electrocardiographic LVH, lower in-treatment Cornell product LVH treated as a time-varying covariate was associated with a 12.4% lower rate of new-onset AF (adjusted hazard ratio [HR], 0.88; 95% CI, 0.80-0.97; P = .007) for every 1050 mm x msec (per 1-SD) lower Cornell product, with persistence of the benefit of losartan vs atenolol therapy on developing AF (HR, 0.83; 95% CI, 0.71-0.97; P = .01). Lower Cornell product electrocardiographic LVH during antihypertensive therapy is associated with a lower likelihood of new-onset AF, independent of blood pressure lowering and treatment modality in essential hypertension. These findings suggest that antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may reduce the incidence of new-onset AF.

Issue Highlights

HomeCirculationVol. 113, No. 12Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published28 Mar 2006https://doi.org/10.1161/circ.113.12.1549Circulation. 2006;113:1549RELATIONSHIP BETWEEN HOMOCYSTEINE AND MORTALITY IN CHRONIC KIDNEY DISEASE, by Menon et al.Prior studies relating plasma homocysteine to the risk of cardiovascular disease in the general population have yielded inconsistent results. Reduced glomerular filtration rate (GFR) is a risk factor for cardiovascular disease, and plasma homocysteine is related inversely to GFR. Therefore, the association of plasma homocysteine with cardiovascular disease in some earlier reports may have been confounded by inadequate adjustment for GFR. In this issue of Circulation, Menon and colleagues relate homocysteine levels to all-cause and cardiovascular mortality in patients with stages 3 to 4 chronic kidney disease enrolled in the Modification of Diet in Renal Disease Study who were followed up for a median duration of 10 years. The authors observed that plasma homocysteine levels increased with worsening GFR. In analyses adjusting for GFR (measured by the renal clearance of 125I-iothalamate), plasma homocysteine was not associated with all-cause or cardiovascular mortality. These observations suggest that plasma homocysteine may be a marker of severity of kidney disease rather than an independent risk factor in patients with stages 3 to 4 chronic kidney disease. See p 1572.IMPACT OF DIABETES MELLITUS ON REGRESSION OF ELECTROCARDIOGRAPHIC LEFT VENTRICULAR HYPERTROPHY AND THE PREDICTION OF OUTCOME DURING ANTIHYPERTENSIVE THERAPY: THE LOSARTAN INTERVENTION FOR ENDPOINT (LIFE) REDUCTION IN HYPERTENSION STUDY, by Okin et al.Research has established that left ventricular hypertrophy (LVH) is associated with excess morbidity and mortality. Moreover, recent observational and randomized data support the concept that LVH regression improves prognosis. Whether the benefits of LVH regression are equivalent across various patient subgroups is, however, uncertain. Dr Okin and colleagues examined over 9000 patients with hypertension in the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study, 1195 of whom had diabetes, to understand the benefits of LVH regression in patients with diabetes. Consistent with prior studies, the investigators observed that the prevalence of LVH was greater among patients with diabetes. However, with a mean follow-up of about 5 years, patients with diabetes had less electrocardiographic LVH regression. Surprisingly, though the mortality benefit of hypertension treatment in diabetes is established, LVH regression per se was not predictive of improved prognosis in those with diabetes. The data of Okin et al suggest that the pathogenesis of the poor prognosis associated with LVH in diabetes is multifactorial and merits further investigation. See p 1588.WOMEN HAVE HIGHER LEFT VENTRICULAR EJECTION FRACTIONS THAN MEN INDEPENDENT OF DIFFERENCES IN LEFT VENTRICULAR VOLUME: THE DALLAS HEART STUDY, by Chung et al.The clinical utility of ejection fraction is widely accepted, and despite the well-recognized pitfalls, it remains an important predictor of outcome in multiple different cardiac diseases. In general, common cutpoints have been applied to men and women. In this week’s journal, Chung et al acquired cardiac magnetic resonance imaging in 1435 women and 1183 men from the Dallas Heart Study. This carefully performed study in a probability-based sample of Dallas residents aged 30 to 65 demonstrated that the median left ventricular ejection fraction in women (75%) is higher than in men (70%); this is secondary to a higher stroke volume. This gender-associated difference in stroke volume is independent of end-diastolic volume and other evaluated confounders. Future work will be needed to assess the importance of this finding in the study of cardiovascular diseases. See p 1597.Visit http://circ.ahajournals.org:Clinician UpdateGastrointestinal Complications of Dual Antiplatelet Therapy. See p e655.Images in Cardiovascular MedicineSevere Left Atrial Edema and Heart Failure After Atrial Fibrillation Ablation. See p e659.Serial High-Spatial-Resolution, Multisequence Magnetic Resonance Imaging Studies Identify Fibrous Cap Rupture and Penetrating Ulcer Into Carotid Atherosclerotic Plaque. See p e660.Diffuse Infiltration of Lymphoma of the Myocardium Mimicking Clinical Hypertrophic Cardiomyopathy. See p e662. Download figureDownload PowerPointCorrespondenceSee p e665. Previous Back to top Next FiguresReferencesRelatedDetails March 28, 2006Vol 113, Issue 12 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.113.12.1549 Originally publishedMarch 28, 2006 PDF download Advertisement

Association of electrocardiographic left ventricular hypertrophy with the incidence of new congestive heart failure.

To investigate the association of electrocardiographic (ECG) left ventricular hypertrophy (LVH) with the incidence of new congestive heart failure (CHF) in older people. In a prospective study of 2638 older people, ECGs were obtained at study entry, at 1 month after study entry, when clinically indicated, and at least yearly after study entry. ECG LVH was diagnosed if the point score of Romhilt and Estes was > or = 5. Persistent LVH was diagnosed if all of the ECGs showed LVH. New LVH was diagnosed if the baseline ECG showed no LVH but LVH was present on the last ECG. Regression of LVH was diagnosed if the baseline ECG showed LVH but no LVH was present on the last ECG. No LVH was diagnosed if all of the ECGs showed no LVH. Persistent LVH, new LVH, regression of LVH, and no LVH were correlated with the incidence of new CHF at follow-up. A large long-term health care facility. The patients included 1805 women and 833 men, mean age 81 +/- 9 years (range 60 to 103). Of the 2,638 older persons studied, 281 (11%) had persistent ECG LVH, 31 (1%) had new ECG LVH, 12 (0.5%) had regression of ECG LVH, and 2314 (88%) had no ECG LVH. At 42 +/- 24 months (range 1 to 154 months) follow-up, new CHF developed in 168 of 281 persons (60%) with persistent LVH, in 16 of 31 persons (52%) with new LVH, in 4 of 12 persons (33%) with regression of LVH, and in 507 of 2314 persons (22%) with no LVH. Kaplan-Meier survival curves showed that the development of new CHF was higher in persons with persistent LVH versus regression of LVH (P = .013), in persons with persistent LVH versus no LVH (P = .001), in persons with new LVH versus regression of LVH (P = .039), and in persons with new LVH versus no LVH (P = .001). Older persons with persistent or new ECG LVH have a higher incidence of new CHF and an earlier time to the development of new CHF than older persons without ECG LVH.

Effect of beta-blockade on exercise capacity in hypertensive subjects: A one-year double-blind study of celiprolol and metoprolol

To assess the effect of beta-blocker antihypertensive therapy on exercise capacity, 40 patients randomized to celiprolol 200 mg and metoprolol 100 mg daily in a double-blind fashion were studied after a month of placebo and a year of active treatment. Both drugs normalized office blood pressure and produced echocardiographic and electrocardiographic left ventricular hypertrophy regression. In symptom-limited maximal stress tests before and after treatment, exercise duration increased with (p < 0.0001) celiprolol (513-700 seconds) and metoprolol (520-634 seconds), although more with the former (p = 0.02). Resting heart rate was reduced with both, more with metoprolol (p < 0.001), while heart rate at peak exercise was reduced similarly with both medications (p < 0.005). Blood pressure at peak exercise was reduced with both celiprolol (217-184 mmHg; p = 0.0002) and metoprolol (218-185 mmHg, p < 0.0001) to a similar degree (p = NS). Exercise parameters were not related to patient age or the degree of left ventricular hypertrophy regression (p = NS). It is concluded that beta-blocker antihypertensive therapy improves exercise capacity, decreasing heart rate and blood pressure responses to stress, irrespective of left ventricular structural changes.