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PubMed2005

[Rationale, characteristics and study design of PREAMI (Perindopril and Remodelling in the Elderly with Acute Myocardial Infraction)].

Angiotensin-converting enzyme (ACE) inhibitors reduce mortality and morbidity in patients with heart failure and/or left ventricular systolic dysfunction and in patients with acute myocardial infarction (AMI), especially those with heart failure and/or evidence of left ventricular systolic dysfunction. ACE-inhibitors prevent cardiac events in patients at high cardiovascular risk and/or with documented coronary artery disease. There is a lack of data on the role of ACE-inhibitors in the elderly population with AMI and preserved left ventricular function. Nevertheless, the issue is of primary importance, considering the median age of patients with AMI and heart failure, the high risk of death, heart failure and left ventricular remodeling in the elderly, and the progressive aging of the general population. The multicenter and international (109 centers from five European countries), double-blind, randomized, parallel PREAMI (Perindopril and Remodelling in the Elderly with Acute Myocardial Infarction) trial evaluated the effects of the ACE-inhibitor perindopril in the elderly (aged > or =65 years) with AMI and preserved or mildly depressed left ventricular systolic function (ejection fraction > 40%). The combined primary endpoint was death, hospitalization for heart failure, and left ventricular remodeling (considered as an increase in left ventricular end-diastolic volume > or = 8%). Secondary endpoints included: each single primary endpoint, cardiovascular death, hospitalization for reinfarction or angina, and revascularization. The study involved 1252 patients, with an average age of 73 years, and AMI, treated with recommended usual therapy (antithrombotic drugs, beta-blockers, ACE-inhibitors). After 11 +/- 4 days from AMI, patients were randomized to receive either perindopril (4 mg/day for the first month and 8 mg/day for the remaining 11 months) or placebo, in addition to the recommended conventional therapy. Clinical assessment was performed at fixed times and included two-dimensional echocardiography (to evaluate left ventricular remodeling), Holter electrocardiographic monitoring (to assess heart rate variability and arrhythmias), and blood sampling (for safety evaluation). This review provides details on the background, rationale and study design of PREAMI.

Age Factors↗
PubMed2000

N-terminal proatrial natriuretic peptide and prognosis in patients with heart failure and preserved systolic function.

BACKGROUND: Congestive heart failure and preserved left ventricular systolic function is a common clinical condition. Although the prognosis in this type of heart failure is better in comparison to systolic dysfunction, prognostic markers to evaluate long-term outcome are lacking. The atrial peptide, N-terminal proatrial natriuretic peptide (proANP), has been shown to predict survival in patients with systolic dysfunction. We intended to evaluate the predictive capability of N-terminal proANP in patients with preserved systolic function (ejection fraction [EF] > or = 0.40). METHODS AND RESULTS: A clinical and echocardiographic examination was performed in 149 patients with idiopathic heart failure from a population-based cohort, and 84 patients were identified to have preserved systolic function, with an EF of 0.40 or greater. The patients were followed up during 7 years with regard to symptoms, treatment, hospitalization, and survival. The patients with normal EFs had greater plasma concentrations of N-terminal proANP compared with a control group, and N-terminal proANP level was an independent predictor of mortality (risk ratio, 2.44; 95% confidence interval, 1.28 to 4.67; P = .007). In addition, a high concentration of N-terminal proANP predicted an increased rate of hospitalization (50% for a level > 1,200 pmol/L versus 19% for a level < or = 1,200 pmol/L; P = .046) and a greater future dosage of diuretic (127+/-102 vs 51+/-39 mg; P = .007). CONCLUSION: N-terminal proANP level was an independent marker of increased mortality and morbidity in patients with preserved systolic function, whereas EF was not usable in this regard. It is suggested that this peptide could be used to identify clinically relevant left ventricular dysfunction in patients with EFs within the normal range.

Aged↗
PubMed2005

[Systolic ventricular dysfunction, a new marker of coronary artery disease in patients with aortic stenosis without previous myocardial infarction].

Identification of clinical factors associated with coronary artery disease could obviate the need for coronary angiography in selected patients with severe aortic stenosis. We studied 315 patients (68 [8] years) with severe aortic stenosis without previous infarction who underwent coronary angiography. In the univariate analysis, age (P = .001), dyslipidemia (P = .003), angina (P = .018), aortic gradient (P = .001) and reduced ejection fraction (P = .006) were predictors of coronary artery disease. After multivariate analysis, age (OR = 1.079, P = .01), ejection fraction < 40% (OR = 2.685, P = .02), angina (OR = 2.518, P = .04) and dyslipidemia (OR = 2.34, P = .008) were the factors independently associated with coronary artery disease. Left ventricular dysfunction correlated independently with the presence of coronary artery disease.

Aged↗
PubMed2000

[Diastolic heart failure. Physiopathology].

BACKGROUND: Systolic dysfunction of the left ventricle is not the only mechanism of heart failure. An increasing number of patients are found to have heart failure with an ejection fraction > or = 40%. The proportion of heart failure patients with "diastolic" (or more appropriately preserved systolic function) heart failure increases with age. This clinical entity currently accounts for 30 to 40% of all hospitalizations for heart failure and in patients over 80 is found in more patients than is systolic dysfunction. PATHOPHYSIOLOGY: Diastolic heart failure generally associates prolonged ventricular relaxation with reduced left ventricular capacity for distention. The main causes are ischemic, hypertensive and age-related heart disease. Concentric remodeling of the left ventricle, with or without hypertrophy, always leads to diastolic functional disorders. A triggering factor is almost always found for episodes of acute congestion. CONCLUSION: The incidence of "diastolic" heart failure increases with age. Physicians should be aware of the complex underlying pathophysiological mechanisms.

Adult↗
PubMed1998

[Heart failure after myocardial infarction: diagnosis, treatment, prevention. Echocardiography should be a routine procedure in myocardial infarction].

Post-infarction prognosis is considerably impaired if left ventricular systolic dysfunction and/or symptomatic heart failure develops. As the symptoms of left ventricular dysfunction are often subtle or completely lacking, such patients can be identified only by objective evaluation of left ventricular function. However, as symptoms of heart failure may develop despite normal left ventricular function, objective evaluation of left ventricular function is also important in symptomatic patients, since prognosis is especially poor in the presence of systolic dysfunction. As echocardiography is the most suitable and accessible method in the context, also allowing assessment of cardiac dimensions and valvular function, its extended use in post-infarction patients is imperative. Left ventricular dysfunction should be prevented by adequate measures to limit the extent of infarction and prevent its recurrence. To improve prognosis, the use of ACE (angiotensin converting enzyme) inhibitors should be considered whenever left ventricular dysfunction is present, irrespective of symptomatology. Treatment with amiodarone has recently been shown to reduce mortality among patients with post-infarction heart failure, and should also be considered in such cases, especially if there is a need of antiarrhythmic therapy. Although beta-receptor blockers have well-documented beneficial effects in myocardial infarction, their effect on patients with latent or overt heart failure has not been specifically studied. The use of angiotensin II antagonists in patients with post-infarction heart failure or left ventricular dysfunction is currently under investigation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Cost-effectiveness of eplerenone compared with placebo in patients with myocardial infarction complicated by left ventricular dysfunction and heart failure.

BACKGROUND: In the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), aldosterone blockade with eplerenone decreased mortality in patients with left ventricular systolic dysfunction and heart failure after acute myocardial infarction. The present study was performed to evaluate the cost-effectiveness of eplerenone compared with placebo in these patients. METHODS AND RESULTS: A total of 6632 patients with left ventricular systolic dysfunction and heart failure after acute myocardial infarction were randomized to eplerenone or placebo and followed up for a mean of 16 months. The coprimary end points were all-cause mortality and the composite of cardiovascular mortality/cardiovascular hospitalization. The evaluation of resource use included hospitalizations, outpatient services, and medications. Eplerenone was priced at the average wholesale price, 3.60 dollars per day. Survival beyond the trial period was estimated from data from the Framingham Heart Study, the Saskatchewan Health database, and the Worcester Heart Attack Registry. The incremental cost-effectiveness of eplerenone in cost per life-year and quality-adjusted life-year gained compared with placebo was estimated. The number of life-years gained with eplerenone was 0.1014 based on Framingham (95% CI, 0.0306 to 0.1740), 0.0636 with Saskatchewan (95% CI, 0.0229 to 0.1038), and 0.1337 with Worcester (95% CI, 0.0438 to 0.2252) data. Cost was 1391 dollars higher over the trial period in the eplerenone arm (95% CI, 656 to 2165) because of drug cost. The incremental cost-effectiveness ratio was 13,718 dollars per life-year gained with Framingham (96.7% under 50,000 dollars per life-year gained), 21,876 dollars with Saskatchewan, and 10,402 dollars with Worcester. CONCLUSIONS: Eplerenone compared with placebo in the treatment of heart failure after acute myocardial infarction is effective in reducing mortality and is cost-effective in increasing years of life by commonly used criteria.

Aged↗
PubMed1994

Left ventricular diastolic dysfunction.

Diastolic heart failure is common, particularly in patients with coronary artery disease and hypertension. Although it does not contribute to heart failure mortality to the same degree as systolic dysfunction, it is responsible for significant morbidity. Clinical suspicion is a prerequisite to the diagnosis, which should be considered in all patients with exercise intolerance due to dyspnoea, particularly if associated with a history of ischaemic heart disease or hypertension. Although invasive haemodynamic studies are the gold standard investigation, this method of assessment is limited to a very small proportion of these patients, and echocardiography remains the single most useful investigation. It is important to realize that the management of diastolic heart disease depends to a large extent on the aetiology, which contrasts with the treatment of systolic dysfunction. As indicated, a wide variety of different drugs may potentially be of benefit, although considerable further research will be needed to more clearly define this heterogenous condition and its optimal treatment.

Diastole↗
PubMed2003

Effect of the Asp298 variant of endothelial nitric oxide synthase on survival for patients with congestive heart failure.

BACKGROUND: Significant variation exists within the endothelial nitric oxide synthase (NOS3) gene that may influence cardiovascular risk. The Asp298 variant of NOS3 has a shorter half-life in endothelial cells. Given the importance of nitric oxide in the heart failure syndrome, we evaluated the effect of this variant on event-free survival in a population with systolic dysfunction. METHODS AND RESULTS: Four hundred sixty-nine patients (72% male, 49% ischemic; mean age, 56+/-12 years) with systolic dysfunction (left ventricular ejection fraction < or =0.45) were enrolled in a study of Genetic Risk Assessment of Cardiac Events (GRACE). The polymorphism in exon 7 of NOS3, a G-T transition at position 894 that results in a Glu to Asp amino acid substitution for codon 298, was genotyped and subjects were followed prospectively to the end point of death or heart transplantation. Event-free survival was compared on the basis of the presence (group 1, n=266) or absence (group 2, n=203) of the Asp298 variant. Event-free survival was significantly poorer in patients with the Asp298 variant (percent event-free survival group 1 at 1/2/3 years=78/65/54; group 2=82/72/64, P=0.03). In subset analysis, the adverse impact of the Asp298 variant was primarily in patients with nonischemic cardiomyopathy (group 1=82/73/63; group 2=87/79/71, P=0.03) and was not apparent among patients with ischemic heart disease (group 1=75/59/47; group 2=74/62/54, P=0.71). CONCLUSIONS: For patients with heart failure caused by systolic function, the Asp298 variant of NOS3 is associated with poorer event-free survival, particularly in patients with nonischemic cardiomyopathy.

Adult↗
PubMed1999

Costs associated with symptomatic systolic heart failure.

OBJECTIVE: To investigate whether the extent of systolic dysfunction is a useful predictor of the costs of healthcare and social support for patients with heart failure. DESIGN: Cross-sectional study with collection of cost data attributed to management of heart failure in the previous year. SETTING: Four primary-care practices in Scotland. PATIENTS: Patients receiving long term therapy with loop diuretics for suspected heart failure. INTERVENTIONS: Two-dimensional and Doppler echocardiography. MAIN OUTCOME MEASURES AND RESULTS: Two hypotheses were tested: (i) the proportion of patients incurring costs is higher in patients with abnormal left ventricular (LV) function; and (ii) the median cost per patient that incurs costs is higher in patients with abnormal LV function. Of the 226 patients in the study, 67 (30%) had abnormal systolic function. In comparison with the remaining 159 patients, they had higher healthcare costs [560 Pounds vs 440 Pounds per patient year (1994/1995 values)], were more likely to incur hospital inpatient or outpatient costs [Odds ratio (OR): 2.02; 95% confidence interval (CI): 1.06 to 3.84] and had significantly higher primary-care costs (mean 292 Pounds vs 231 Pounds per patient year; p = 0.02, Mann Whitney test). In contrast, they were no more likely to incur social support costs (OR: 1.22; 95% CI: 0.52 to 2.86) and the mean cost of social support per patient year was lower (234 Pounds vs 373 Pounds). CONCLUSIONS: Patients with objectively measured systolic dysfunction incurred significantly higher healthcare costs in the year before diagnosis. This suggests that treatment that improves systolic function will reduce healthcare costs, even in a primary-care population with relatively mild congestive heart failure.

Cross-Sectional Studies↗
PubMed1993

From Left Ventricular Dysfunction to Heart Failure in the Elderly Patient.

The pathophysiology of the syndrome of congestive heart failure (CHF) is different in elderly patients compared to middle-aged subjects. When the syndrome of CHF predominantly results from left ventricular (LV) systolic dysfunction, peripheral mechanisms in elderly patients are less apt to compensate for the decline in LV performance due to deconditioning of the skeletal muscles, decreased vasodilatory response to exercise, and reduced capacity to excrete sodium. These all develop with age. LV diastolic dysfunction, i.e., LV filling impairment, appears to be a more frequent cause of CHF in elderly patients than in middle-aged subjects. Hypertrophy of the cardiac myocyte is associated with a prolongation of the calcium transient which, in turn, results from a decreased concentration of the enzyme responsible for reuptake of calcium in the sarcoplasmic reticulum. Cardiac myocyte hypertrophy results from a steady loss of myocytes and a progressive rise in arterial impedance which are both observed with aging. Notwithstanding subendocardial myocardial ischemia which is frequently associated with LV wall hypertrophy, prolongation of the calcium transient leads to impaired LV wall relaxation and the syndrome of LV diastolic dysfunction. The goals of therapy are also different in elderly patients compared to middle-aged patients. In elderly patients, one is less concerned about restoring a near normal exercise capacity, and aims at preventing acute episodes of decompensation which frequently accompany excessive sodium intake. Therefore, strict adherence to diet and careful titration of the dosages of medication to renal function are important considerations when treating CHF in elderly patients. In particular, cardiac glycosides, which should be avoided with CHF due to LV diastolic dysfunction, should be carefully titrated to creatinine clearance and body weight when treating elderly patients with LV systolic dysfunction in sinus rhythm. Similarly, the dosages of most angiotensin-converting enzyme inhibitors should be reduced in elderly patients.

Journal Article↗
PubMed1999

Doppler echocardiographic study in adolescents and young adults with sickle cell anemia.

OBJECTIVE: Anatomical and functional assessment of the heart through Doppler and echocardiography in patients with cell anemia (SCA). METHODS: Twenty-five patients with SCA and ages ranging from 14 to 45 years were prospectively studied in a comparison with 25 healthy volunteers. All of them underwent clinical and laboratory evaluation and Doppler echocardiography as well. The measurements were converted into body surface indices. RESULTS: There were increases in all chamber diameters and left ventricle (LV) mass of the SCA patients. It was characterised an eccentric hypertrophy of the left ventricle. The preload was increased (left ventricle end-diastolic volume) and the afterload was decreased (diastolic blood pressure, peripheral vascular resistance and end-systolic parietal stress ESPS). The cardiac index was increased due to the stroke volume. The ejection fraction and the percentage of the systolic shortening, as well as the systolic time intervals of the LV were equivalent. The isovolumetric contraction period of the LV was increased. The mitral E-septum distance and the end-systolic volume index (ESVi) were increased. The ESPS/ESVi ratio,a loading independent parameter, was decreased in SCA, suggesting systolic dysfunction. No significant differences in the diastolic function or in the pulmonary pressure occurred. CONCLUSION: Chamber dilations, eccentric hypertrophy and systolic dysfunction confirm the evidence of the literature in characterizing a sickle cell anemia cardiomyopathy.

Adolescent↗
PubMed2006

Guillain-Barré syndrome as a cause of reversible cardiomyopathy.

Although autonomic dysfunction is a common manifestation of Guillain-Barré syndrome, cardiovascular involvement in this setting has rarely been reported in the literature. We describe a case of reversible left ventricular systolic dysfunction in a 60-year-old man with Guillain-Barré syndrome. Our patient had no history or signs of cardiac dysfunction on initial presentation. During the clinical manifestation of his autonomic dysfunction, he developed electrocardiographic changes accompanied by mildly elevated cardiac enzymes and severe left ventricular systolic dysfunction and segmental wall motion abnormality, which coincided with elevated urinary catecholamine and vanilmandelic acid levels. These abnormalities, and his symptoms, resolved rapidly once the acute episode was over. We believe the reversible left ventricular dysfunction was due to the toxic effect of increased catecholamines and to the transiently damaged sympathetic nerve endings in the myocardium, presumably a consequence of Guillain-Barré syndrome. We recommend that echocardiography be performed in patients with clinical signs of autonomic dysfunction, especially if they are associated with abnormal electrocardiographic findings, cardiac enzyme elevation, or hemodynamic instability, so that appropriate medical therapy can be instituted in a timely manner.

Guillain-Barre Syndrome↗
PubMed1997

Can the clinical examination diagnose left-sided heart failure in adults?

We systematically reviewed the literature to ascertain how well clinicians determine the probability and type of left-sided heart failure in their patients. Left-sided heart failure is characterized by decreased left ventricular ejection fraction or increased filling pressure. The type of heart failure determines optimal treatment. Systolic dysfunction exists when ejection fraction is reduced. Diastolic dysfunction is presumed to be present when filling pressure is increased with a normal ejection fraction and without another explanatory diagnosis. Many findings are associated with heart failure, and wide variation exists in clinicians' ability to detect these findings. The best findings for detecting increased filling pressure are jugular venous distention and radiographic redistribution. The best findings for detecting systolic dysfunction are abnormal apical impulse, radiographic cardiomegaly, and q waves or left bundle branch block on an electrocardiogram. Diastolic dysfunction is especially difficult to diagnose, but is associated with an elevated blood pressure during heart failure.

Clinical Competence↗
PubMed2004

The prognosis of impaired left ventricular systolic function and heart failure in a middle-aged and elderly population in an urban population segment of Copenhagen.

AIMS: To determine the prognosis, total mortality and cardiac morbidity, of patients with left ventricular systolic dysfunction and heart failure (HF) in a general population sample. METHODS AND RESULTS: A total of 764 subjects, 432 females and 332 males, median age (range) 66 years (50-89), participated in this cross sectional survey. The study population was recruited from randomly selected general practitioners and stratified to include a minimum of 150 persons in each age decade stratum. Each participant filled in a heart failure questionnaire and ECG, blood tests and echocardiography were performed. Median (range) follow-up was 1145 (51-1197) days. Subjects with LVEF < or = 0.40 had a significantly higher all-cause mortality (27.8% vs. 5.6%, P<0.0001), admission rate for HF (25.0% vs. 1.9%, P<0.0001) and for other cardiac causes (25.0% vs. 6.3%, P<0.0001) than in subjects with LVEF>0.40. The age and gender adjusted 2-year relative risk of death was 4.6 (95% C.I.=1.6-13.2). No significant difference in mortality was found between subjects with or without heart failure symptoms. CONCLUSION: Significantly higher mortality as well as cardiac morbidity was found in subjects with symptomatic and asymptomatic LV systolic dysfunction compared to those with normal systolic function. These conditions were among the strongest predictors of all-cause mortality and cardiac morbidity.

Aged↗
PubMed1992

Implications of third heart sounds in patients with valvular heart disease. The Veterans Affairs Cooperative Study on Valvular Heart Disease.

BACKGROUND: The presence of third heart sounds in patients with valvular heart disease is often regarded as a sign of heart failure, but it may also depend on the type of valvular disease. METHODS: We assessed the prevalence of third heart sounds and the relation between third heart sounds and cardiac function in 1281 patients with six types of valvular heart disease. RESULTS: The prevalence of third heart sounds was higher in patients with mitral regurgitation (46 percent) or aortic regurgitation (28 percent) than in those with aortic stenosis (11 percent) or mitral stenosis (8 percent). The left ventricular ejection fraction was significantly lower (P less than 0.001) when a third heart sound was detected in patients with aortic stenosis (0.38, vs. 0.56 in those without third heart sounds) or mixed aortic valve disease (0.40 vs. 0.55). However, the ejection fraction was only slightly lower in patients with mitral regurgitation and third heart sounds (0.51 vs. 0.57, P = 0.03). The pulmonary-capillary wedge pressure was higher (P less than 0.001) when a third heart sound was detected in patients with aortic stenosis (18.6 mm Hg, vs. 12.1 mm Hg in those without third heart sounds). There was no association between the wedge pressure and third heart sounds in patients with mitral regurgitation. The prevalence of third heart sounds increased with the severity of mitral regurgitation. CONCLUSIONS: In patients with mitral regurgitation, third heart sounds are common but do not necessarily reflect left ventricular systolic dysfunction or increased filling pressure. In patients with aortic stenosis, third heart sounds are uncommon but usually indicate the presence of systolic dysfunction and elevated filling pressure.

Adult↗
PubMed2002

Cardiovascular effects of successful renal transplantation: a 1-year sequential study of left ventricular morphology and function, and 24-hour blood pressure profile.

BACKGROUND: Cardiovascular disease is the leading cause of death in renal transplant recipients. The purpose of this study was to determine the effects of a successful renal transplantation on left ventricular morphology and function and on the 24-hr blood pressure profile. METHODS: Twenty-four patients with end-stage renal disease were prospectively studied by ambulatory blood pressure monitoring and echocardiography before and at 3, 6, and 12 months after renal transplantation. Patients were also analyzed according to their renal function after transplantation. RESULTS: We observed a significant drop in the mean values of daytime and nocturnal systolic blood pressure and in the 24-hr systolic pressure load at 12 months after transplantation. The most frequent echocardiographic finding was left ventricular hypertrophy (LVH), for which the incidence decreased from 75% before transplantation to 52.1% at 12 months after transplantation (P = 0.125). There was a significant decrease in left ventricular dilatation, and systolic dysfunction normalized in all patients after 12 months. The variables that best independently predicted the decrease in LVH were serum creatinine levels and the 24-hr systolic pressure load as registered by ambulatory blood pressure monitoring at 12 months after transplantation. We observed significant decreases in left ventricular mass and left ventricular mass index in the group of patients who had adequate renal function, as compared with no changes in patients who did not. CONCLUSIONS: Correction of the uremic state by renal transplantation leads to complete resolution of systolic dysfunction, regression of LVH, and improvement of left ventricular dilatation. In fact the reduction of LVH was dependent on adequate renal function and on a decrease in the systolic pressure levels.

Adult↗
PubMed1995

Systolic ventricular dysfunction and heart failure due to coronary microangiopathy in hypertensive heart disease.

Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.

Antihypertensive Agents↗
PubMed2006

[Hypertension and heart].

The term hypertensive heart disease covers the entities left ventricular hypertrophy, microangiopathy, diastolic and systolic dysfunction, und increased risk of arrhythmias. From the pathophysiological point of view this is caused by hypertrophy of cardiac myocytes, interstitial fibrosis and media hypertrophy of the arterioles. As an earliest sign of hypertensive heart disease a microangiopathy can be diagnosed. Also a diastolic dysfunction can be found as an early change. In further persisting arterial hypertension left ventricular hypertrophy develops (often asymmetric), and later a systolic dysfunction. Clinically, the patients suffer from angina pectoris, dyspnea and rhythm disorders. Left ventricular hypertrophy is associated with an increased risk of ventricular malignant arrhythmias. Thus, the main therapeutic principle should be antihypertensive therapy with the goal of regression of hypertrophy and, as a consequence, a decreased mortality risk.

Arrhythmias, Cardiac↗