edited by Ihor Gussak, and Charles Antzelevitch, coedited by Stephen C. Hammill, Win‐Kuang Shen, Preben Bjerregaard. Humana Press Inc., Totowa, New Jersey, 2003
Abstract— Left ventricular hypertrophy (LVH), a marker of cardiac end-organ damage, is a common complication of hypertension. Regression of LVH is achievable by sustained lowering of systolic blood pressure (BP). However, it is unknown whether a strategy aimed at lowering BP beyond that recommended would lower the risk of LVH. We examined the effect of intensive (systolic BP<120 mm Hg), compared with standard (systolic BP<140 mm Hg), BP lowering on the risk of LVH in 4331 patients with diabetes mellitus from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) BP trial, a randomized controlled trial. The outcome measures were electrocardiographic LVH defined by Cornell voltage (binary variable) and mean Cornell index (continuous variable). The baseline prevalence of LVH (5.3% versus 5.4%; P =0.91) and the mean Cornell index (1456 versus 1470 µV; P =0.45) were similar in the intensive (n=2154) and standard (n=2177) BP-lowering arms, respectively. However, after median follow-up of 4.4 years, intensive, compared with standard, BP lowering was associated with a 39% lower risk of LVH (odds ratio [95% confidence interval], 0.61[0.43, 0.88]; P =0.008) and a significantly lower adjusted mean Cornell index (1352 versus 1447 µV; P <0.001). The lower risk of LVH associated with intensive BP lowering during follow-up was because of more regression of baseline LVH and lower rate of developing new LVH, compared with standard BP lowering. No interactions by age, sex, or race were observed. These results provide evidence that targeting a systolic BP of <120 mm Hg when compared with <140 mm Hg in patients with hypertension and diabetes mellitus produces a greater reduction in LVH. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00000620
Background The purpose of this investigation was to establish normal values of RR variability for middle-aged persons and compare them with values found in patients early and late after myocardial infarction. We hypothesized that presence or absence of coronary heart disease, age, and sex (in this order of importance) are all correlated with RR variability. Methods and Results To determine normal values for RR variability in middle-aged persons, we recruited a sample of 274 healthy persons 40 to 69 years old. To determine the effect of acute myocardial infarction RR variability, we compared measurements of RR variability made 2 weeks after myocardial infarction (n=684) with measurements made on age- and sex-matched middle-aged subjects with no history of cardiovascular disease (n=274). To determine the extent of recovery of RR variability after myocardial infarction, we compared measurements of RR variability made in the group of healthy middle-aged persons with measurements made in 278 patients studied 1 year after myocardial infarction. We performed power spectral analyses on continuous 24-hour ECG recordings to quantify total power, ultralow-frequency (ULF) power, very-low-frequency (VLF) power, low-frequency (LF) power, high-frequency (HF) power, and the ratio of LF to HF (LF/HF) power. Time-domain measures also were calculated. All measures of RR variability were significantly and substantially lower in patients with chronic or subacute coronary heart disease than in healthy subjects. The difference from normal values was much greater 2 weeks after myocardial infarction than 1 year after infarction, but the fractional distribution of total power into its four component bands was similar for the three groups. In healthy subjects, ULF power did not change significantly with age; VLF, LF, and HF power decreased significantly as age increased. Patients with chronic coronary heart disease showed little relation between power spectral measures of RR variability and age. Patients with a recent myocardial infarction showed a strong inverse relation between VLF, LF, and HF power and age and a weak inverse relation between ULF power and age. ULF power best separates the healthy group from either of the two coronary heart disease groups. Differences in RR variability between men and women were small and inconsistent among the three groups. Conclusions All measures of RR variability were significantly and substantially higher in healthy subjects than in patients with chronic or subacute coronary heart disease. The difference between healthy middle-aged persons and those with coronary heart disease was much greater 2 weeks after myocardial infarction than 1 year after infarction, but the fractional distribution of total power into its four component bands was similar for the healthy group and the two coronary heart disease groups. Values of RR variability previously reported to predict death in patients with known chronic coronary heart disease are rarely (≈1%) found in healthy middle-aged individuals. Thus, when measures of RR variability are used to screen groups of middle-aged persons to identify individuals who have substantial risk of coronary deaths or arrhythmic events, misclassification of healthy middle-aged persons should be rare.
Editorials1 August 1984How Do Beta-Blockers Protect After Myocardial Infarction?J. THOMAS BIGGER JR., M.D., JAMES COROMILAS, M.D.J. THOMAS BIGGER JR., M.D., JAMES COROMILAS, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-101-2-256 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSeveral large, double-blind, randomized, placebo-controlled clinical trials have shown that beta-adrenergic blocking drugs reduce the mortality rate and incidence of nonfatal myocardial infarction in the first 2 years after myocardial infarction (1). The most impressive evidence of their benefit comes from the Beta-Blocker Heart Attack Trial (2) and a Norwegian trial with timolol (3). Both studies were analyzed by the intention-to-treat principle, even though dropout rates were substantial (4).In the Norwegian study (3), 1884 patients were randomly assigned to receive placebo or timolol maleate, 10 mg twice daily, 7 to 28 days after infarction, and continued treatment for an...References1. FRISHMANFURBERGFRIEDEWALD WCW. Beta-adrenergic blockade for survivors of acute myocardial infarction. N Engl J Med. 1984;310:830-7. CrossrefMedlineGoogle Scholar2. . A randomized trial of propranolol in patients with acute myocardial infarction: I. Mortality results. JAMA. 1982;247:1707-14. CrossrefMedlineGoogle Scholar3. . Timolol-induced reduction in mortality and reinfarction in patients surviving acute myocardial infarction. N Engl J Med. 1981;304:801-7. CrossrefMedlineGoogle Scholar4. PETOPIKEARMITAGE RMP. Design and analysis of randomized clinical trials requiring prolonged observation of each patient: I. Introduction and design. Br J Cancer. 1976;34:585-612. 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Author, Article, and Disclosure InformationAffiliations: Columbia University New York, New York PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAcute electrophysiologic consequences of pyridostigmine inhibition of cholinesterase in humansPrevention of ventricular fibrillation requires central β-adrenoceptor blockade in rabbitsCholinergic stimulation with pyridostigmine reduces the QTc interval in coronary artery diseaseBETA-ADRENERGIC BLOCKING AGENTS IN THE TREATMENT OF CONGESTIVE HEART FAILURE: Mechanisms and Clinical ResultsHeart rate and blood pressure variability in cardiac diseases: pharmacological implicationsEffect of Beta Adrenergic Receptor Blockade on Cardiac Autonomic Tone in Patients with Chronic Stable AnginaBeta blockers in heart failureTHE CARDIAC ION CHANNELS: Relevance to Management of ArrhythmiasInfarct size estimated from peak creatine kinase is reduced in patients using beta-blockers at the onset of chest painBeta-blockers in heart failure: Promising or proved?Effect of atenolol and diltiazem on heart period variability in normal personsEffects of transdermal scopolamine on heart rate variability in normal subjectsInfluence of Ischemia and Infarction on Cardiac Vagal and Sympathetic InnervationSympathetic Denervation, Supersensitivity, and Arrhythmogenesis After Myocardial InfarctionEffect of intravenous metoprolol on left ventricular performance in Q-wave acute myocardial infarctionPrognostic significance of ventricular ectopic activity in survivors of acute myocardial infarction who receive propranololCurrent approaches to drug treatment of ventricular arrhythmiasPostinfarction anginaCALCIUM ANTAGONISTS AND ISCHAEMIC HEART DISEASEResults of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.Decreased heart rate variability and its association with increased mortality after acute myocardial infarctionElectrocardiographic and ventriculographic recovery patterns in Q wave myocardial infarctionEffect of propranolol in patients with myocardial infarction and ventricular arrhythmiaWhy do beta-receptor blockers decrease mortality after myocardial infarction? 1 August 1984Volume 101, Issue 2Page: 256-258KeywordsClinical trialsDeath ratesDrugsHeartInfarctionIntent to treat analysisLongitudinal studiesLungsMyocardial infarctionRespiratory system procedures Issue Published: 1 August 1984 PDF downloadLoading ...
