Treatment Of Left Ventricular Hypertrophy Research Articles

January 7/14, 2003

HomeCirculationVol. 107, No. 1January 7/14, 2003 Free AccessAnnouncementPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAnnouncementPDF/EPUBJanuary 7/14, 2003 James T. Willerson, MD James T. WillersonJames T. Willerson Search for more papers by this author Originally published7 Jan 2003https://doi.org/10.1161/circ.107.1.1Circulation. 2003;107:1Circulation’s Newest Section Mini-Reviews: Expert OpinionsDr Dean Kereiakes is the Section Editor for Circulation’s newest section, Mini-Reviews: Expert Opinions. Expert opinions and advice will be solicited from internationally recognized thought-leaders for topics in cardiovascular medicine that are of interest to the cardiovascular clinician. In addition, health-care policy and patient care issues will be examined attempting to improve clinical care and resource utilization. Mini-Reviews: Expert Opinions will provide timely, useful advice on the recognition and management of important cardiovascular problems and will expand the clinically relevant format of Circulation. The new section will be available in print and via a radio button on the home page of Circulation Online in January 2003.Circulation’s Ongoing New Features: Clinician Update and The Cardiology Patient PageDr Elliott Antman is Section Editor for two new sections that were introduced in the Online version of Circulation in May 2001. The sections are available as a collection through radio buttons on the home page of Circulation Online, and now the Clinician Update is also published in the print journal. We are pleased to offer the new sections as a review for the clinician and as a resource for the patient.Rapid Track for Review and PublicationThe Rapid Track category of manuscript is designed to provide expedited review within 7 working days and, if accepted, rapid publication of manuscripts reporting the results of important clinical trials and major basic science discoveries. Accepted manuscripts are published online within 7 to 10 working days and within 4 to 5 weeks in the print journal after return of the corrected proofs. If an author believes his/her work meets the criteria for the Rapid Track consideration as stated in our Instructions to Authors, the author should request Rapid Track consideration in the submission letter that accompanies the manuscript.Rapid Access PublicationAll original manuscripts accepted for publication in Circulation are now published Online in our Rapid Access Publication Section one week after proofs are returned to Lippincott Williams & Wilkins and are in print in five weeks. The Online section is available via a radio button on Circulation’s home page.Cardiovascular NewsImages in Cardiovascular MedicineThromboembolism in Real-Time Two-Dimensional EchocardiographyGershan K. Davis, MD, MRCP, FRACP; Clive Fisk, MTO; Sandeep Talwar, PhD, MRCP (Circulation. 2003; 107:e1Google Scholar.) Cardiology Patient PageExercise and Cardiovascular HealthJonathan Myers, PhD (Circulation. 2003; 107:e2-e5Google Scholar.) Correspondence (Circulation. 2003; 107:e6-e13Google Scholar.) Previous Back to top Next FiguresReferencesRelatedDetailsCited By Meetoo D, Ochieng B and Fatani T (2014) Deep vein thrombosis: an underestimated threat, Journal of Operating Department Practitioners, 10.12968/jodp.2014.2.7.323, 2:7, (323-329), Online publication date: 2-Nov-2014. O'rourke T, Slagle W, Elkins M, Eckermann D and Musick A (2021) Papilloedema associated with dural venous sinus thrombosis, Clinical and Experimental Optometry, 10.1111/cxo.12092, 97:2, (133-139), Online publication date: 1-Mar-2014. Blacher J, Agnoletti D, Protogerou A, Iaria P, Czernichow S, Zhang Y and Safar M (2011) Aortic stiffness, inflammation, denutrition and prognosis in the oldest people, Journal of Human Hypertension, 10.1038/jhh.2011.73, 26:9, (518-524), Online publication date: 1-Sep-2012. Crespo-Leiro M and Hermida-Prieto M (2008) Sirolimus treatment of left ventricular hypertrophy: who, and when?, European Heart Journal, 10.1093/eurheartj/ehn470, 29:22, (2703-2704) Reusch F, Scheid M, Beckmann A, Gassel A and Krian A (2008) Therapie einer fulminanten Lungenembolie mit seltener Koinzidenz unter Einsatz der extrakorporalen Membranoxygenierung (ECMO)Pulmonary embolism of rare coincidence under employment of extracorporeal-membrane-oxygenation system (ECMO), Zeitschrift für Herz-,Thorax- und Gefäßchirurgie, 10.1007/s00398-008-0612-x, 22:1, (32-35), Online publication date: 1-Feb-2008. January 7, 2003Vol 107, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.107.1.1 Originally publishedJanuary 7, 2003 PDF download Advertisement

Fabry disease: focus on cardiac manifestations and molecular mechanisms.

Fabry disease is an inherited lysosomal storage disorder caused by deficiency of the enzyme alpha-galactosidase A. The enzyme deficiency results in accumulation of glycosphingolipids in the lysosomes n nearly all cell types and tissues leading to a multisystem disease. MANIFESTATIONS include painful crisis, angiokeratomas, corneal dystrophy, and hypohydrosis. The severe renal, cerebrovascular, and cardiac involvement is predominantly responsible for premature mortality in Fabry patients. The disease is X-linked and manifests primarily in hemizygous males but also heterozygous females can be affected. CARDIAC INVOLVEMENT is frequent in Fabry disease. Patients develop hypertrophic cardiomyopathy, arrhythmias, conduction abnormalities, and valvular abnormalities. Although Fabry disease leads to a complex clinical syndrome, there are studies indicating that manifestations can be limited to the heart. The isolated cardiac variant of Fabry disease seems to be more common than previously thought: around 3-6% of male patients with left ventricular hypertrophy seem to suffer from this disease variant. Recent advances in molecular biology and genetic engineering have enabled the development of enzyme replacement therapy in Fabry disease. Results from two independent therapy studies are indeed promising: Infusion of the enzyme preparation seems to be well tolerated and effective in catabolizing the lipid deposits. This enzyme replacement therapy could be one of the first examples for causal treatment of left ventricular hypertrophy. Therefore, early diagnosis of hypertrophy patients with the cardiac variant of Fabry disease is important.

The spironolactone renaissance

Until recently, spironolactone was considered only as an antagonist at the aldosterone receptors of the epithelial cells of the kidney and was used clinically in the treatment of hyperaldosteronism and, occasionally, as a K+-sparing diuretic. The spironolactone renaissance started with the experimental finding that spironolactone reversed aldosterone-induced cardiac fibrosis by a cardiac action. Experimentally, spironolactone also has direct effects on blood vessels. Spironolactone reduces vascular fibrosis and injury, inhibits angiogenesis, reduces vascular tone and reduces portal hypertension. The rationale for the Randomized Aldactone Evaluation Study (RALES) of spironolactone in heart failure was that ‘aldosterone escape’ occurred through non-angiotensin II mechanisms. The RALES clinical trial was stopped early when it was shown that there was a 30% reduction in risk of death among the spironolactone patients. In RALES, spironolactone also reduced hospitalisation for worsening heart failure and improved the symptoms of heart failure. Other recent clinical trials have shown that spironolactone reduces cardiac and vascular collagen turnover, improves heart variability, reduces ventricular arrhythmias, improves endothelial dysfunction and dilates blood vessels in human heart failure and these effects probably all contribute to the increased survival in heart failure. Spironolactone may also be useful in the treatment of left ventricular hypertrophy, portal hypertension and cirrhosis. There have also been some recent small clinical trials of spironolactone as an anti-androgen showing potential in acne, hirsutism and precocious puberty.

Optimal antihypertensive therapy for prevention and treatment of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is considered an adaptation to a pressure load on the left ventricle and is common in hypertensive patients. The condition is a profound risk factor for cardiovascular events, greater than and independent of blood pressure. It is now recognized in hypertension management guidelines as an indication for more stringent blood pressure control. All of the first-line antihypertensive agents have been shown to variably regress LVH, but no definitive evidence yet shows that one agent is superior to others in decreasing risk independent of blood pressure control. Although some evidence suggests that reduction of LVH is associated with improved prognosis independent of blood pressure control, relative efficacy of drug classes in this regard has yet to be demonstrated. At present, recommendations for optimal therapy in hypertensive patients with LVH must rest on the presence of underlying cardiac and noncardiac conditions, with the understanding that the major classes of antihypertensive agents will probably decrease LVH.

Epidemiology and treatment of left ventricular hypertrophy in the elderly.

Left ventricular hypertrophy (LVH) is an important independent risk factor for cardiovascular disease and is associated with an increased risk of ventricular dysrhythmia, coronary artery disease, myocardial infarction, stroke, heart failure and peripheral artery disease. The prevalence of LVH increases strongly with advancing age and, consequently, the prevention or reduction of LVH should be an important consideration in the older age-group. This review summarises current knowledge on LVH and discusses management issues with particular reference to the elderly. Evidence suggests that antihypertensive treatment can reverse or prevent LVH. There have been few studies of LVH in the elderly, but since age does not appear to be a factor in the regression of LVH, results of studies among younger hypertensive patients can be extrapolated to the elderly population. Meta-analyses of clinical studies have not established conclusively that angiotensin-converting enzyme inhibitors and calcium antagonists are necessarily more effective than diuretics and beta-adrenoceptor antagonists in reducing LVH.

Echocardiography overestimates left ventricular mass

To compare measurement of left ventricular mass (LVM) by M-mode echocardiography and magnetic resonance imaging (MRI) in hypertensive subjects. A prospective study. Twenty-four untreated hypertensive patients [19 men and five women, aged 51 +/- 2 (mean +/- SEM) years, supine blood pressure 159/101 +/- 3/1 mmHg]. The Blood Pressure Unit, St Georges Hospital Medical School and Magnetic Resonance Unit, Royal Brompton National Heart and Lung Hospital, London. LVM estimated both by M-mode echocardiography and by MRI. Using three standard M-mode formulae, widely different values of LVM were obtained with echocardiography [American Society of Echocardiography (ASE) 319 +/- 21 g, Penn 273 +/- 19 g. Teichholz 191 +/- 11 g]. By MRI, the LVM was 232 +/- 11 g. The differences between MRI and echocardiography could not be explained in terms of the timing of measurements in the cardiac cycle. When single-slice MRI measurements at the appropriate level were applied to the ASE and Penn formulae, the LVM was again overestimated. Our study has shown major differences in LVM estimated using methods based on one-dimensional (echocardiography) compared with three-dimensional (MRI) data. These differences seem to be largely the result of the geometrical assumptions on which M-mode measurements are based. Our findings have important clinical implications for the assessment of the severity and response to treatment of left ventricular hypertrophy in hypertensive patients.

Plasma angiotensin II, predisposition to hypertension, and left ventricular size in healthy young adults.

We studied the correlates of left ventricular mass (LVM) in 84 healthy young adults aged 16 to 24 years from the general population. Subjects were selected according to predisposition to hypertension into four groups with either high or low personal blood pressures and either high or low parental blood pressures. LVM was measured by echocardiography, and measurements of blood pressure, heart rate, body dimensions, and plasma concentrations of components of the renin-angiotensin system were made under resting conditions. LVM was similar in individuals predisposed to hypertension (high personal and parental blood pressures) and those with contrasting predisposition (low personal and parental pressures). Regression analysis of the combined groups showed that LVM correlated closely with body size, particularly lean body mass (r=.69, P<.0001) and systolic (r=.35, P<.0001) but not diastolic blood pressure. Plasma angiotensin II (r=.39, P<.0001), renin (r=.302, P<.01), and angiotensin-converting enzyme (r=.22, P<.05) showed significant correlation with LVM. Multiple regression analysis revealed that plasma angiotensin II was the most important component of the renin-angiotensin system and that its effect was independent of systolic blood pressure and body size. These findings provide evidence in humans that angiotensin II exerts a direct on myocardial size. This association may have important implications for the complications and treatment of left ventricular hypertrophy.

Therapeutic advances in the treatment of left ventricular hypertrophy.

As a consequence of persistently raised blood pressure, left ventricular hypertrophy (LVH) develops as a compensatory mechanism for wall stress induced by the increase in afterload. Recent advances in the fields of molecular biology and genetics are now clarifying the mechanisms involved in the development of LVH. It has been reported that messenger RNA of oncogenes, such as c-fos and c-myc, increases by stretching; these oncogenes contribute to the progression of LVH, the messenger RNA expression of myosin and contractile protein synthesis in the cardiomyocytes. Vasoactive hormones and vascular contracting factors are also reported to have a progressive effect on LVH. In contrast, some antihypertensive agents have been shown to have pharmacological effects on regression of LVH in animals and man. The mechanisms responsible for LVH progression have been extensively studied. In contrast, the mechanisms of LVH regression have not been defined and require elucidation. This paper outlines the basic recognition of the mechanisms of LVH progression and discusses the varied pharmacological actions of calcium antagonists and angiotensin converting enzyme inhibitors on the regression of LVH in man and rats. Although the role of antihypertensive therapy in regression of LVH remains controversial, the calcium antagonist nicardipine appears to have an important role to play in the treatment of LVH in hypertension and in congestive heart failure.

Left ventricular hypertrophy.

To review the pathophysiology, epidemiology, patterns, diagnosis, and treatment of left ventricular hypertrophy with emphasis on the elderly. A computer-assisted search of the English-language literature (MEDLINE database) followed by a manual search of the bibliographies of pertinent articles. Studies on the pathophysiology, epidemiology, patterns, diagnosis, and treatment of left ventricular hypertrophy were screened for review. Studies on left ventricular hypertrophy in the elderly and recent studies were emphasized. Pertinent data were extracted from the reviewed articles. Emphasis was on studies involving the elderly. Relevant articles were reviewed in depth. Available data about the pathophysiology, epidemiology, patterns, diagnosis, and treatment of left ventricular hypertrophy with emphasis on studies involving the elderly were summarized. Left ventricular hypertrophy caused by hypertension or other cardiovascular disease is not only a marker for but also a contributor to cardiovascular morbidity and mortality in elderly and young patients. The question of whether regression of left ventricular mass in patients with hypertension will decrease cardiovascular morbidity and mortality needs to be answered by prospective studies using different types of antihypertensive drugs. Future studies on the efficacy of antihypertensive drugs and on stratification of therapy should include echocardiographic estimates of left ventricular mass index.