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Therapeutic implications of marine omega-3 highly unsaturated fatty acids (HUFA) in cardiovascular disease are still discussed controversially. Several clinical trials report divergent findings and thus leave ambiguity on the meaning of oral omega-3 therapy. Potential prognostic indications of HUFA treatment have been predominantly studied in coronary artery disease, sudden cardiac death, ventricular arrhythmias, atrial fibrillation and heart failure of various origin. It is suspected that increased ventricular wall stress is crucially involved in the prognosis of heart failure. Increased wall stress and an unfavorable myocardial remodeling is associated with an increased risk of arrhythmias by stretch-activated membrane ion channels. Integration of HUFA into the microenvironment of cardiomyocyte ion channels lead to allosteric changes and increase the electrical stability. Increased ventricular wall stress appears to be involved in the local myocardial as well as in the hepatic fatty acid metabolism, i.e. a cardio-hepatic syndrome. Influences of an altered endogenous HUFA metabolism and an inverse shift of the fatty acid profile was underrated in the past. A better understanding of these interacting endogenous mechanisms appears to be required for interpreting the findings of recent experimental and clinical studies. The present article critically reviews major studies on basic pathophysiological mechanisms and treatment effects in clinical trials., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: In several trials, beneficial prognostic effects of highly unsaturated fatty acids (HUFAs) in heart failure were shown. Because other studies showed no incremental benefit in nearly preserved cardiac function, the question arises, whether the degree of cardiac dysfunction is involved. It is hypothesized that increased left ventricular (LV) wall stress affects the endogenous hepatic HUFA metabolism, which in turn exhibits adverse cardiac consequences., Methods: Cardiac magnetic resonance imaging was performed in 30 patients with suspected cardiomyopathy. The serum fatty acid profile was assessed using gas chromatography/mass spectrometry., Results: Docosahexaenoic acid (DHA; P = 0.002) and eicosapentaenoic acid (EPA; by trend) levels were decreased in patients with reduced LV ejection fraction (≤ 50%) or LV dilatation (≥ 90 mL/m(2)). Decreased DHA (P = 0.003) and EPA (P = 0.022) levels were associated with a reduced LV ejection fraction. Decreased DHA level was correlated with increased end-diastolic (P = 0.047) and end-systolic LV wall stress (P = 0.001). Pseudocholinesterase activity was inversely correlated with end-diastolic (P = 0.020) and end-systolic LV wall stress (P = 0.025)., Conclusions: DHA level was significantly reduced in heart failure. Similar, but less pronounced effects were found for EPA and arachidonic acid by trend. Increased LV wall stress was correlated with a reduced DHA level. Increased LV wall stress exhibits various adverse consequences (eg, increased oxygen consumption, favouring of arrhythmias, and an unfavourable remodelling). The increase of wall stress was paralleled by reduced HUFA level. Increased LV wall stress was correlated with reduced pseudocholinesterase, which is suggestive of hepatic congestion (ie, a cardiohepatic syndrome, involved in the altered fatty acid profile in heart failure) and has major consequences regarding the dose-efficacy of HUFA treatment., (Copyright © 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Background: COPD and heart failure occur with a considerable coincidence. Beside well-known mechanisms of increased right heart load in COPD, dedicated changes of the left ventricle (LV) are ill-defined and the question remains, whether specific interactions exist beyond common shared risk factors., Methods: LV wall stress was calculated based on cardiac magnetic resonance imaging in 28 patients with COPD (GOLD I to III) and coexistent heart failure (LVEF 42 ± 19%) due to non-ischaemic and ischaemic cardiomyopathy., Results: LV enddiastolic (p = 0.048) and endsystolic wall stress (p = 0.034) increased from GOLD stage I to III. Reduced FEV1 was correlated with increased enddiastolic (p = 0.0210) and endsystolic LV volume (p = 0.0413) and with increased enddiastolic (p = 0.0161) and endsystolic LV wall stress (p = 0.0315), respectively. Increased wall stress was associated with a decreased FEV1/FVC ratio., Conclusions: The severity of airflow limitation in COPD was correlated with increased LV wall stress. It is suggested that respiration in pulmonary obstruction is associated with an increased negative intrathoracic pressure when compared with normal lung function, which is transmitted to the heart and increases the transmural pressure gradient and thereby distending forces on the heart. Increased ventricular wall stress is known to be associated with a broad variety of unfavourable consequences, which should be taken into account to contribute to a worse prognosis in COPD., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Objectives: To explore the rationale for ω-3 fatty acids in heart failure treatment, the dosage of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) for replacing low levels of highly unsaturated fatty acids (HUFA deficiency) was examined. To judge the usefulness of various EPA/DHA preparations, their content of peroxides and aldehydes was determined., Methods: In 298 patients with dilative heart failure, the serum HUFA level was assessed by gas chromatography. In ω-3-acid ethyl esters 90 (Omacor/Lovaza, approved by the Food and Drug Administration and the European Medicines Agency) and 63 dietary supplement fish oils, oxidation products were determined by photometry., Results: Increasing serum HUFA from the lower (4.3 ± 1.0%) to the upper (9.5 ± 1.5%) tertile would be associated with an increased left ventricular (LV) ejection fraction (34.1 ± 9.9 vs. 28.3 ± 9.5%, p < 0.01) and reduced LV enddiastolic diameter (63.5 ± 7.1 vs. 66.9 ± 7.4 mm) requiring at least 2 g EPA/DHA daily. In fish oils, the peroxide and alkenal level varied greatly, i.e. peroxide value ≤ 5 mEq/kg in only 7 and ≤ 10 mEq/kg in 38 fish oils. Compared with equivalent doses of ω-3-acid ethyl esters 90, the mean peroxide intake would be 8.6 ± 6.1 and the alkenal intake 10.9 ± 4.4 times higher in fish oils., Conclusions: Levels of adverse oxidation products should be considered when targeting HUFA deficiency or treating patients with myocardial infarction or high triglycerides., (Copyright © 2013 S. Karger AG, Basel.)

Introduction: To examine a potential interrelation of left ventricular (LV) wall stress and hypertrophy, we assessed increased wall stress in patients with suspected non-ischemic dilative cardiomyopathy and addressed the question whether increased LV wall stress is involved in the development of LV hypertrophy., Methods: We studied 502 consecutive patients in whom LV mass, LV enddiastolic (LVEDV) and endsystolic volume (LVESV) was determined using cardiac magnetic resonance (CMR). Based on a thick-walled sphere, we introduced a myocardial and cavity volume-based wall stress index. Follow up CMR examinations were obtained in a representative subgroup of 71 patients., Results: LV mass was correlated with LVEDV (r=0.517, P<0.001) and LVESV (r=0.510, P<0.001). Despite LV hypertrophy, LV mass was not sufficient to compensate for LV dilatation resulting in an increased wall stress. Increased LV enddiastolic wall stress was found in 227 patients (45 %) and increased endsystolic wall stress in 198 (39 %). In patients with normal LV enddiastolic wall stress ≤ 4 kPa at time of enrolment, no changes of LV mass occurred during follow up (142 ± 46 g vs. 141 ± 47 g). In contrast, patients with initially increased LV enddiastolic wall stress >4 kPa developed greater LV hypertrophy (141 ± 48 g vs. 158 ± 60 g, P=0.0247)., Conclusions: LV wall stress can be derived from CMR measurements of LV myocardium and cavity using the volume-based wall stress index. Increased LV enddiastolic wall stress leads to LV hypertrophy. Beyond a certain degree of LV dilatation, the extent of hypertrophy does not compensate LV dilatation. The ensuing increased wall stress promotes dilatation and consecutively hypertrophy with an unfavorable prognosis. It is proposed to use the volume-based wall stress index as new diagnostic criterion in heart failure., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

The causes of reduced levels of omega-3 and omega-6 highly unsaturated fatty acids ("HUFA deficiency") in heart failure remain unresolved. HUFA profiles were examined in the serum of 331 patients with failing versus nonfailing heart disease. Arachidonic acid was positively correlated (P < 0.001) with eicosapentaenoic acid (EPA) (r = 0.40) and docosahexaenoic acid (DHA) (r = 0.53) and negatively with palmitic (r = 0.42), palmitoleic (r = 0.38), and oleic acid (r = 0.48). Delta-5 desaturase activity was reduced (P < 0.01) in heart failure patients with low ejection fraction, dilatation, increased wall stress, and reduced heart rate variability (SDNN). In these patients, the reduced (P < 0.01) HUFA and increased palmitic (P < 0.01) and oleic acid (P = 0.05) arose from separate influences involving reduced cardiac contractility (arachidonic acid and palmitic acid predicted by ejection fraction) and chamber dilatation (DHA and oleic acid predicted by end-diastolic diameter). A low DHA (0.2%-0.9% versus 1.4%-3.1%) was associated (P < 0.025) with atrial dilatation (44 ± 8 mm versus 40 ± 8 mm). Equidirectional but less pronounced effects on HUFA were induced by sympathetic activation and (or) insulin resistance (fat and sugar fed to deoxycorticosterone acetate (DOCA)-salt rats) but not by compensated cardiac overload alone (DOCA-salt or aortic constriction), or reduced fatty acid oxidation (CPT-1 inhibition). Based on administration of omega-3 HUFA (OMACOR), dilatation is identified as a target for 1-2 g omega-3 HUFA·day(-1). Interventions for reduced arachidonic acid remain to be explored.

Background: Sudden cardiac death of suspected healthy young athletes is a rare, but deeply moving event. Usually, the affected person has been completely free of symptoms. Commonly, unrecognized inflammatory, hypertrophic or dilated cardiomyopathies are the most frequent causes. All therapeutic principles of angiotensin-converting-enzyme (ACE) inhibition, beta-blockade, and diuretics in heart failure aim to unload the heart. During physical activity increased sympathetic tonus and loading conditions for the heart point into the opposite direction. This raises the question to what extent physical activity in patients with myocarditis, dilated cardiomyopathy or heart failure in general is tolerable., Synopsis: Several experimental studies revealed disadvantages of physical exercise during acute myocarditis leading to an increase in mortality. On the other hand, several small trials in men demonstrate an improvement of physical fitness and quality of life attributed to controlled supervised exercise training in patients with heart failure without assessment of mortality. Dilated cardiomyopathy was diagnosed in one third of these patients. There was no biopsy confirmation of these conditions. The other two thirds of patients suffered from ischemic heart diseases., Conclusion: Since the borderline between inflammatory heart disease and noninflammatory or postinflammatory dilated cardiomyopathy is difficult to determine, abstention from physical training during and shortly after inflammatory heart disease is recommended, because it is known that viral persistence or autoimmune processes could last for several months.

Definition and Classification: Cardiomyopathies are disorders affecting the heart muscle that frequently result in congestive heart failure. Five major forms are recognized: dilated, hypertrophic, restrictive, right ventricular, and nonclassifiable cardiomyopathies with distinct hemodynamic properties. Furthermore, the new WHO/WHF definition also comprises inflammatory cardiomyopathy, defined as myocarditis in association with cardiac dysfunction. Idiopathic, autoimmune, and infectious forms of inflammatory cardiomyopathy were recognized. Viral cardiomyopathy is defined as viral persistence in a dilated heart. It may be accompanied by myocardial inflammation and then termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). If no inflammation is observed in the biopsy of a dilated heart (< 14 lymphocytes and macrophages/mm2), the term viral cardiomyopathy or viral persistence in dilated cardiomyopathy should be applied., Diagnosis and Treatment: In recent years, there have been breakthroughs in understanding the molecular and genetic mechanisms involved in this group of conditions, enabling improvement of diagnostic strategies and introduction of new therapies. Ongoing evaluation of antiviral, immunoglobulin, and immunosuppressive therapies including the European Study of Epidemiology and Treatment of Cardiac Inflammatory Diseases (ESETCID), removal of antibodies by immunoadsorption, anticytokine and gene therapy, as well as the mechanical support devices may provide new treatment options.

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Introduction Heart failure can be caused by systolic or diastolic dysfunction. Diagnosing diastolic dysfunction remains challenging, although several criteria have been identified. Ventricular wall stress is crucially involved. It is hypothesized whether increased end-diastolic and end-systolic ventricular wall stress as assessed by the wall stress index is associated with cardiac dysfunction and thus provide novel diagnostic criteria. Methods 1050 consecutive patients with suspected non-ischemic heart failure covering a broad spectrum from normal to severely impaired cardiac function were observed. Cardiac magnetic resonance imaging was performed to assess left ventricular (LV) volumes, myocardial mass, peak ejection (PER) and filling rate (PFR). Results A reduced PFR was found in 348 patients (33.1%), which resulted from 275 of 422 patients (65.2%) with reduced and from 73 of 628 patients (11.6%) with preserved LVEF (p < 0.0001). Increased LV volume and mass was correlated with reduced PER and PFR (p < 0.0001). Increased end-diastolic wall stress was the strongest predictor of a reduced PER (OR 4.5 [2.6 to 7.8], p < 0.0001) and increased end-systolic wall stress predicted a reduced PFR (OR 1.2 [1.1 to 1.3], p < 0.0001). Increased end-systolic wall stress was correlated with increased pulmonary pressure (p < 0.0001). Normal end-systolic wall stress < 18 kPa had a favorable predictive value for the absence of an impaired filling and increased pulmonary capillary pressure. Conclusion Increased end-diastolic wall stress precedes a reduced ventricular ejection rate and increased end-systolic wall stress determines an impaired diastolic filling. It is thus suggested to add assessment of ventricular wall stress as diagnostic criterion of heart failure. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aims Occurrence of late gadolinium enhancement (LGE) as assessed by cardiac magnetic resonance (CMR) imaging has been attributed to various myocardial injuries. We hypothesized that LGE is associated with left ventricular (LV) wall stress. Methods and results We examined 300 patients with suspected non-ischaemic dilated cardiomyopathy. Cardiac magnetic resonance was used to assess LV volume, mass, wall stress, and LGE. Increased LV end-diastolic wall stress (> 4 kPa) was found in 112 patients (37 %), and increased end-systolic wall stress (>18 kPa) in 121 patients (40%). Presence of LGE was observed in 93 patients (31%). End-diastolic (94 ± 43 vs. 79 ± 42 ml/m², P = 0.006) and end-systolic LV volumes (62 ± 44 vs. 44 ± 37 ml/m², P < 0.001) and LV mass (95 ± 34 vs. 78 ± 31 g/m², P < 0.001) were increased in patients exhibiting LGE. In particular, LV end-diastolic and end-systolic wall stress were increased (4.5 ± 2.8 vs. 3.6 ± 3.0 kPa, P = 0.025; 19.6 ± 9.1 vs. 17.5 ± 8.2 kPa, P = 0.045). Late gadolinium enhancement was observed more frequently than would be expected from random occurrence in patients with increased end-diastolic (39 vs. 26%, P = 0.020) and end-systolic wall stress (41 vs. 24%, P = 0.002). Both normal end-diastolic and end-systolic wall stress had a high negative predictive value for LGE (75 and 76%). Conclusions The present study shows that occurrence of LGE in cardiomyopathy is associated with increased LV wall stress and mass. Suspected causes are an increased capillary leakage by stretch, impaired contrast agent redistribution, or increased diffusion distances. It is proposed that LGE should be considered as a potential prognostic determinant of heart failure and severe arrhythmias. [ABSTRACT FROM AUTHOR]

Background: Hyperhomocysteinemia is a risk factor for ischemic heart disease. Several other mechanisms apply also to dilative types of heart failure of various, non-ischemic etiologies. We hypothesized that hyperhomocysteinemia is associated with left ventricular (LV) dilatation and hypertrophy in dilative cardiomyopathy. Methods: Homocysteine was measured in 66 individuals with suspected cardiomyopathy. Cardiac magnetic resonance imaging was used to assess LV volume, mass, and wall stress. Results: Hyperhomocysteinemia (>12 μmol/L) was found in 45 patients (68%). LV mass was greater in these patients compared with individuals with normal homocysteine (83±27 vs. 67±19 g/m2; p<0.02). Homocysteine was increased in patients with increased brain natriuretic peptide ≥100 pg/mL (18.3±5.9 vs. 14.9±5.1 μmol/L; p=0.018). LV mass, LV end-diastolic and end-systolic volume (LVEDV, LVESV) were significantly increased in individuals in the upper quartile compared with the lower quartile (90±25 vs. 65±18 g/m2, p=0.021; 114±50 vs. 71±23 mL/m2, p=0.042; 76±51 vs. 36±22 mL/m2, p=0.045). LV dilatation (LVEDV≥90 mL/m2) was more common in hyperhomocysteinemia (>12 μmol/L, p=0.0166). Normalized LV mass was correlated with homocysteine (r=0.346, p=0.065). Homocysteine was not significantly correlated with LVEDV (r=0.229, p=0.065), LV end-diastolic wall stress (r=0.226, p=0.069) and LV ejection fraction. Conclusions: Hyperhomocysteinemia appears to be, at least in part, involved in a disproportional LV dilatation, where the ensuing hypertrophy is not sufficient to compensate for the increased wall stress. A potential mechanism is the hyperhomocysteinemia associated increase in oxidative stress that favors muscle fiber slippage. Clin Chem Lab Med 2010;48:555–60. [ABSTRACT FROM AUTHOR]

Background: Heart failure is characterized by neurohumoral dysfunction that can be assessed by measurement of heart rate variability (HRV). Depression of HRV is related to several hemodynamic parameters. We hypothesized that an increased left ventricular (LV) wall stress is related to a depressed HRV in patients with LV dilatation or dysfunction. Methods: Cardiac function and mass were measured in 31 patients with LV dilatation or dysfunction and 21 controls using cardiac magnetic resonance (CMR) imaging. LV wall stress was calculated using a CMR-based thick-walled sphere model. Standard deviation of normal-to-normal (NN) intervals (SDNN) and average NN intervals over 5 minutes (SDANN-i) were calculated. Results: LV end-diastolic (ED) and end-systolic (ES) wall stress were significantly increased in patients with SDNN < 75 ms (P < 0.05). SDNN and SDANN-i were decreased (P = 0.001, P < 0.001) in patients with LVED wall stress >8 kPa and LVES wall stress >30 kPa (P < 0.05). To examine potential effects of LVEF, LVED and LVES volume, and wall stress on HRV, a multiple linear regression analysis was performed, which revealed LVED wall stress as the only independent parameter influencing SDNN (P = 0.039). LV ejection fraction, LV mass, and volumes were not significantly related to HRV. Conclusions: LV wall stress was independently related with depression of HRV. Therefore, LV wall stress might be prognostically important and a therapeutic target in heart failure. [ABSTRACT FROM AUTHOR]

Abstract: Acromegaly due to growth hormone excess is a rare condition with a prevalence of 60 per million and an incidence of 3–4 per million and year. Increase of morbidity and mortality is predominantly associated with cardiovascular disease. We report on a 73-year-old female patient with a large pericardial effusion. Measurement of growth hormones confirmed the suspected active hyperpituitarism: growth hormone was 11.8ng/ml, insulin-like growth factor-1 was 1401μg/l (normal 5–199μg/l). The patient underwent cardiac magnetic resonance (CMR) imaging to asses systolic and diastolic cardiac function as well as left ventricular (LV) muscle mass. In contrast to initially suspected cardiac hypertrophy, LV mass was 107g (58g/m2) and, thus, not increased (75–175g, normalized 63–95g/m2). Of note, LV volumes were reduced markedly to 60ml (33ml/m2) at enddiastole and 12ml (7ml/m2) at endsystole; accordingly, the LV ejection fraction was 80%. Subsequently, pericardiocentesis was performed. Noteworthy, diastolic filling was not improved subsequently as assessed by follow-up CMR examination. To our best knowledge, occurrence of pericardial effusion has not yet been described in patients with acromegaly. In contrast to an excellent systolic LV function, diastolic impairment was shown. Of note, diastolic dysfunction remained despite pericardiocentesis. Since also constrictive pericarditis did not occur, myocardial disturbances bearing functional resemblance to restrictive filling pattern have to be considered. Since the accuracy of CMR is favourable when compared with other methods, its diagnostic routine use should be taken into account to assess morphology and function of cardiomyopathy in patients with acromegaly. [Copyright &y& Elsevier]

Abstract: Objectives and background: Myocarditis is caused by various agents and autoimmune processes. It is unknown whether viral genome persistence represents inactive remnants of previous infections or whether it is attributed to ongoing adverse processes. The latter also applies to the course of autoimmune myocarditis. One principal candidate for an adverse remodeling is nuclear factor-κB (NFκB). Methods: A total of 93 patients with suspected myocarditis/cardiomyopathy was examined. Hemodynamics were assessed by echocardiography as well as right and left heart catheterization. Endomyocardial biopsies were taken from the left ventricle. Biopsies were examined by immunohistochemistry and PCR for viral genomes. Selective immunostaining of activated NFκB was performed. Results: NFκB was increased in patients with myocarditis when compared with controls (11.1±7.1% vs. 5.0±5.3%, P <0.005) whereas dilated cardiomyopathy showed no significant increase. Patients with myocarditis and preserved left ventricular function exhibited increased activated NFκB when compared with reduced function (r 2 =0.72, P <0.001). In parallel, inverse correlation of NFκB and left ventricular enddiasstolic volume was found (r 2 =0.43, P <0.02). Increased activated NFκB was found in adenovirus persistence when compared with controls (P =0.001). Only a trend of increased NFκB activation was seen in cytomegalovirus persistence. Parvovirus B19 persistence did not affect NFκB activation. Conclusions: Increased activation of NFκB is related to inflammatory processes in myocarditis. Since activated NFκB correlates with left ventricular function, it could be assumed that NFκB activation occurs at early stages of inflammation. Potentially, NFκB could inhibit loss of cardiomyocytes by apoptosis and protect from cardiac dilation. Since NFκB is a crucial key transcription factor of inflammation, its prognostic and future therapeutic relevance should be addressed. [Copyright &y& Elsevier]

Acquired ventricular septal defects (VSD) are rare and devastating complications after myocardial infarction. The long-term prognosis with medical therapy is extremely poor. We report on a patient who developed progressive heart failure within 3 months after myocardial infarction due to an unknown VSD. The left ventricular function was severely impaired. After diagnosing VSD by echocardiography, surgical occlusion was performed. In addition, a biventricular pacemaker was applied using epicardial leads. The patient recovered almost completely 6 weeks postoperative. Beside hemodynamic changes, biventricular pacing is potentially sufficient to improve the postoperative outcome of patients with severe heart failure in these conditions. [Copyright &y& Elsevier]

Abstract: A 23-year old male (199 cm, 88 kg) presented muscular weakness due to skeletal myopathy and symptoms of heart failure NYHA functional class II. Total creatine kinase was increased up to 830 U/l, but troponin was negative. Prior episodes of intermittent atrial fibrillation were reported and 6 years ago splenectomy was performed due to hereditary spherocytosis. Cardiac magnetic resonance imaging revealed the spongy appearance of non-compacted left ventricular myocardium. This impaired fetal morphogenesis occurred predominantly in the apical to midventricular anterior, lateral and inferior segments. Non-compaction cardiomyopathy was initially described in paediatric patients. Occasional associations with other congenital disorders are known, e.g., Barth syndrome, which is an X-linked disease characterized by cardio-skeletal myopathy of variable severity and neutropenia. To our knowledge, combined occurrence of non-compaction cardiomyopathy, skeletal myopathy and hereditary spherocytosis has not previously been reported. [Copyright &y& Elsevier]

Aims of the Study: To examine the patterns of use, complication rates, and survival in elderly recipients of implantable cardioverter defibrillators (ICD). Methods and Results: We followed 500 consecutive patients included in the Marburg Defibrillator database for 48± 39 months. There were 40 patients (8%) ≥75 and 460 (92%) <75 years of age at the time of implant. The 5-year Kaplan-Meier estimate for appropriate treatment of VT or VF by ICD was 49% among patients <75- versus 57% among patients ≥75-years-old (P = 0.17). The 5-year sudden death rate was similarly low in both groups of patients (2% versus 3%). The 5-year overall mortality rate was significantly higher in patients ≥75 than in patients <75 years of age (55% versus 21%, P = 0.001), due to a higher mortality from heart failure (HF). All procedure-related, lead-related, and pulse generator-related complications were similar in both patient groups (23% versus 25%). Conclusions: ICD therapy was equally effective in patients ≥75 and patients <75 years of age in the prevention of sudden cardiac death. While the complication rates were similar in both age groups, the long-term mortality was considerably higher in elderly patients, due to a higher mortality from HF. The current ICD therapy guidelines appear applicable to elderly patients who are otherwise medically stable and without advanced HF. [ABSTRACT FROM AUTHOR]