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PubMed1993

Heart rate, ischaemic heart disease, and sudden cardiac death in middle-aged British men.

OBJECTIVE: To examine the relation between resting heart rate and new major ischaemic heart disease events in middle aged men with and without pre-existing ischaemic heart disease. DESIGN: Prospective study of a cohort of men with eight years follow up for cardiovascular morbidity and mortality for all men. SETTING: General practices in 24 British towns (the British Regional Heart study). SUBJECTS: 7735 men aged 40-59 years drawn at random from the age-sex registers of one general practice in each town. MAIN OUTCOME MEASURES: Major ischaemic heart disease events such as sudden cardiac death, other deaths attributed to ischaemic heart disease, and non-fatal myocardial infarction. RESULTS: During the follow up period of eight years, 488 men had a major ischaemic heart disease event (217 fatal and 271 non-fatal). Of these, 117 were classified as sudden cardiac death (death within one hour of the start of symptoms). The relation between heart rate and risk of all major ischaemic heart disease events, ischaemic heart disease deaths, and sudden cardiac death was examined separately in men with and without pre-existing ischaemic heart disease. In men with no evidence of ischaemic heart disease, there was a strong positive association between resting heart rate and age adjusted rates of all major ischaemic heart disease events (fatal and non-fatal), ischaemic heart disease deaths, and sudden cardiac death. This association remained significant even after adjustment for age, systolic blood pressure, blood cholesterol, smoking, social class, heavy drinking, and physical activity, with particularly high risk in those with heart rate > or = 90 beats/min. The increased risk seen in those with increased heart rate was largely due to a significantly increased risk of sudden cardiac death, which was five times higher than in those with heart rate < 60 beats/min. The effect of heart rate on sudden cardiac death was present irrespective of blood pressure or smoking state. In men with pre-existing ischaemic heart disease a positive association was seen between raised heart rate and risk of all major ischaemic heart disease events, ischaemic heart disease death, and sudden cardiac death, but the effect was less noticeable than in men without pre-existing ischaemic heart disease. CONCLUSION: In this study of middle aged British men increased heart rate > or = 90 beats/min) is a risk factor for fatal ischaemic heart disease events but particularly for sudden cardiac death. The effect is not dependent on the presence of other established coronary risk factors and is most clearly seen in men free of pre-existing ischaemic heart disease at initial examination.

Adult↗
PubMed2006

ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons.

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Adolescent↗
PubMed2005

Rationale and design of the Optimal Macro-Nutrient Intake Heart Trial to Prevent Heart Disease (OMNI-Heart).

BACKGROUND: The DASH (Dietary Approaches to Stop Hypertension) diet is a carbohydrate-rich, reduced-fat diet that lowers blood pressure (BP) and LDL-cholesterol. Whether partial replacement of some carbohydrate (C) with either protein (P) or unsaturated fat (U) can further improve these and other cardiovascular (CVD) risk factors is unknown. METHODS: OmniHeart is a randomized, three-period, crossover feeding study designed to compare the effects on BP and blood lipids of a carbohydrate-rich diet (CARB, similar to the DASH diet) with a diet rich in protein (PROT, predominantly from nonmeat sources) and a diet rich in unsaturated fat (UNSAT, predominantly monounsaturated). Throughout feeding (run in and the three intervention periods), participants are provided with all of their meals that meet the nutrient profile of their assigned diet. Calorie intake is adjusted to maintain weight. The target sample size is 160 (50% African-American). Participants are adults, aged 30 or older, with prehypertension or Stage 1 hypertension (systolic BP 120-159 or diastolic BP 80-99 mmHg). The primary outcome variables are systolic BP and LDL-cholesterol. Secondary outcomes are diastolic BP, HDL-cholesterol, and triglycerides. Other outcome variables are total cholesterol, apolipoproteins VLDL-apoB, VLDL-apoCIII, apolipoprotein B, non-HDL cholesterol, and lipoprotein(a), and insulin resistance, as measured by Homeostasis Model Assessment (HOMA). CONCLUSIONS: OMNI-Heart should advance our fundamental knowledge of the effects of diet on both traditional and emerging risk factors, and, in the process, guide policy makers, health care providers and the general public on the relative benefits of carbohydrate, protein, and unsaturated fat as a means to reduce CVD risk.

Adult↗
PubMed1978

Reconstruction of mammalian heart tissue from embryonic heart cell suspension with reference to the aggregation of adult heart cells.

Aggregations of isolated embryonic and adult heart cells were studied so as to examine in detail the formation of cell contacts, the assembly of cells into multicellular systems, and cell co-operation in forming organized and differentiating tissues. At selected intervals after initiating rotation cultures, aggregates were examined microscopically for evidence of contractility, and subsequently processed for scanning and transmission electron microscopy (TEM, SEM). By continuous accretion of single cells, and the joining of small clusters, the aggregates increased in size. Cells within the aggregates exhibited rhythmic and synchronous contractility by 3--12 h of culture, suggesting the formation of low-resistance inter-cellular junctions between apposed cells. Two populations of cells could be recognized by 9--12 h with SEM. One was spherical in surface view and the other was flattened. Spherical cells possessed myofibrils, and were classified as cardiac myocytes which occupied the core of the aggregate. The flattened cells were devoid of myofibrils and non-muscle in nature. They covered the surface in a multilayered epithelium. At 12h the aggregates were round to oval, covered by flattened cells, but individual round cells could still be recognized. Intercalated discs were frequently observed in 12 h aggregates. The junctional complexes observed in 12--72 h aggregates include desmosomes, fascia adherens and gap junctions. Most of the aggregation was completed by 24 h, and at later time periods, i.e. 48--72 h, the external surface of the aggregates was smoothed out with epithelial investment. In these aggregates myofibrils and intercellular junctions became reconstructed in less than 24 h. Unlike embryonic myocardial cells, adult cells did not form aggregates of numerous cells. Instead, they formed irregular clusters of 2--5 cells during 3--48 h of culture. Intercellular contacts and suggestive desmosomal materials were observed between adherent cardiac muscle cells. When culture continued for 48--72 h, the cells underwent supercontraction and became non-viable, suggesting that the terminally differentiated adult myocardial cells are incapable of regenerating constituents obligatory for histogenetic reconstruction.

Animals↗
PubMed1996

Analysis of right ventricular function during bypass of the left side of the heart by afterload alterations in both normal and failing hearts.

This study investigated the mechanism of right ventricular failure during bypass of the left side of the heart by precisely assessing right ventricular function with use of a conductance catheter. Bypass of the left side of the heart was established with a centrifugal pump in 10 mongrel dogs weighing 11 to 19 kg. Right ventricular function during left heart bypass was evaluated by two parameters that were both derived from measurement of relative change in right ventricular volume by the conductance catheter technique. One parameter was the right ventricular end-systolic pressure-volume relationship as a load-independent index, and the other was the peak right ventricular pressure-right ventricular stroke volume relationship as a "force-velocity relationship." These parameters were measured in both normal and failing hearts while afterload was increased by bilateral intrapulmonary balloon inflation. Moreover, changes in these relationships were observed by varying assist ratios of left heart bypass from 0% to 100%. Failing heart models were induced by normothermic aortic clamping for 20 minutes. The right ventricular end-systolic pressure-volume relationship in normal hearts did not change, irrespective of the assist ratio of left heart bypass, whereas that in failing hearts decreased from 4.25 +/- 1.41 mm Hg/ml without bypass of the left side of the heart to 3.53 +/- 1.30 mm Hg/ml after 100% assist of left heart bypass (p < 0.05). In the peak right ventricular pressure-right ventricular stroke volume relationship, right ventricular stroke volume was almost constant in normal hearts when afterload was increased regardless of the assist ratio of left heart bypass. Moreover, right ventricular stroke volume was maintained at a higher level during bypass of the left side of the heart compared with that without left heart bypass. However, that slope of the relationship in failing hearts was inversely linear and became significantly steeper after 100% assist of bypass of the left side of the heart compared with that without left heart bypass (-0.131 +/- 0.042 versus -0.051 +/- 0.038, p < 0.005). Therefore ++these two slopes of the relationship intersected at a point that was considered the critical point of afterload during bypass of the left side of the heart. In other words, right ventricular stroke volume was decreased by 100% left heart bypass above the critical point of afterload. In conclusion, this study demonstrates not only that bypass of the left side of the heart results in an increase in right ventricular stroke volume in both normal and failing hearts at the physiologic range of afterload, but also that right ventricular function against higher afterload is impaired by 100% assist of bypass of the left side of the heart in failing hearts.

Animals↗
PubMed1996

Impaired heart rate response to graded exercise. Prognostic implications of chronotropic incompetence in the Framingham Heart Study.

BACKGROUND: Previous reports have suggested that an attenuated exercise heart rate response may be associated with coronary heart disease risk and with mortality. These observations may parallel the association between reduced heart rate variability during normal activities and adverse outcome. This investigation was designed to look at the prognostic implications of exercise heart rate response in a population-based sample. METHODS AND RESULTS: In this prospective cohort investigation, 1575 male participants (mean age, 43 years) in the Framingham Offspring Study who were free of coronary heart disease, who were not taking beta-blockers, and who underwent submaximal treadmill exercise testing (Bruce protocol) were studied. Heart rate response was assessed in three ways: (1) failure to achieve 85% of the age-predicted maximum heart rate, which has been the traditional definition of chronotropic incompetence; (2) the actual increase in heart rate from rest to peak exercise; and (3) the ratio of heart rate to metabolic reserve used by stage 2 of exercise ("chronotropic response index"). Proportional hazards analyses were used to evaluate the associations of heart rate responses with all-cause mortality and with coronary heart disease incidence during 7.7 years of follow-up. Failure to achieve target heart rate occurred in 327 (21%) subjects. During follow-up there were 55 deaths (14 caused by coronary heart disease) and 95 cases of incident coronary heart disease. Failure to achieve target heart rate, a smaller increase in heart rate with exercise, and the chronotropic response index were predictive of total mortality and incident coronary heart disease (P <.01). Failure to achieve target heart rate remained predictive of incident coronary heart disease even after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors (adjusted hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74; P=.02). After adjusting for the same factors, the increase in exercise heart rate remained inversely predictive of total mortality (P=.04) and coronary heart disease incidence (P=.0003). The chronotropic response index also was predictive of total mortality (P=.05) and incident coronary heart disease (P=.001) after adjusting for age and other risk factors. CONCLUSIONS: An attenuated heart rate response to exercise, a manifestation of chronotropic incompetence, is predictive of increased mortality and coronary heart disease incidence.

Adult↗
PubMed1997

Fractal component of variability of heart rate and systolic blood pressure in congestive heart failure.

1. There is a substantial non-harmonic or fractal component to the variability of both heart rate and blood pressure in normal subjects. Heart rate is the more complex of these two signals, with respect to the slope, beta, of the 1/f beta relationship. In congestive heart failure, heart rate spectral power is attenuated, but the fractal and harmonic components of heart rate and systolic blood pressure variability have not been characterized. 2. Two groups, each comprising 20 men, were studied during 15 min of supine rest and spontaneous respiration: one with functional class II-IV heart failure (age 52 +/- 2 years; mean +/- SEM) and a second group of healthy men (age 46 +/- 2 years). 3. Total spectral power for heart rate was significantly reduced in heart failure (P < 0.02), whereas total spectral power for systolic blood pressure was similar in the two groups. In both heart failure and normal subjects, 65-80% of total spectral power in these two signals displayed fractal characteristics. 4. In heart failure, the slope of the 1/f beta relationship for heart rate was significantly steeper than in normal subjects (1.40 +/- 0.08 compared with 1.14 +/- 0.05; P < 0.05), indicating reduced complexity of the fractal component of heart rate variability. There was no significant difference in the 1/f beta slope for systolic blood pressure variability between these two groups, but the blood pressure signals were less complex than heart rate variations in both heart failure (2.31 +/- 0.15; P < 0.006) and normal subjects (2.47 +/- 0.15; P < 0.0001). 5. Parasympathetic nervous system activity, as estimated from heart rate variability was reduced (P < 0.01) in patients with heart failure, whereas trends towards increased sympathetic nervous system activity and decreased non-harmonic power were not significant. 6. The non-harmonic components of cardiac frequency are reduced in heart failure. Non-harmonic power is not attenuated, but the complexity of the heart rate signal is less than in subjects with normal ventricular function. A reduction in parasympathetic modulation appears to contribute to this loss of complexity of heart rate. Consequently, the heart rate signal comes to resemble that of blood pressure. In contrast, the variability and complexity of the systolic blood pressure signal is similar in heart failure and normal subjects. This reduced complexity of heart rate variability may have adverse implications for patients with heart failure.

Blood Pressure↗
PubMed1994

Heart rate variability and its relation to ventricular arrhythmias in congestive heart failure.

BACKGROUND: It has been shown that heart rate variability is decreased in patients with congestive heart failure and that depressed heart rate variability is associated with a propensity to ventricular arrhythmias. Little is known, however, about heart rate variability in patients with both congestive heart failure and ventricular arrhythmias. METHODS: Spectral heart rate variability was analysed from 24 hour ambulatory electrocardiograms in 15 controls, 15 patients with non-sustained ventricular tachycardia associated with clinically normal hearts (NHVT group), and 40 patients with congestive heart failure (CHF group) secondary to either ischaemic heart disease (n = 15) or idiopathic dilated cardiomyopathy (n = 25). Of the 40 patients with congestive heart failure 15 had no appreciable ventricular arrhythmias (ventricular extrasystoles < 10 beats/h and no salvos) and formed the CHF-VA- group. Another 15 patients with congestive heart failure and non-sustained ventricular tachycardia formed the CHF-NSVT group. RESULTS: Heart rate variability was significantly lower in the CHF group than in controls (mean (SD) total frequency 23 (12) v 43 (13) ms; low frequency 12 (8) v 28 (9) ms; high frequency 8 (5) v 14 (7) ms; p < 0.001). The differences in heart rate variability between controls and the NHVT group, between ischaemic heart disease and dilated cardiomyopathy, and between the CHF-VA- and CHF-NSVT groups were not significant. In the CHF group heart rate variability was significantly related to left ventricular ejection fraction but not associated with ventricular arrhythmias. The frequency of ventricular extrasystoles was significantly related to the high frequency component of heart rate variability (r = 0.54, p < 0.05) in the NHVT group. Stepwise multiple regression analysis showed that in the CHF group, heart rate variability was predominantly related to left ventricular ejection fraction (p < 0.05). There was no significant difference in heart rate variability between survivors (n = 34) and those who died suddenly (n = 6) at one year of follow up in the CHF group. CONCLUSION: In patients with congestive heart failure, heart rate variability is significantly decreased. The depressed heart rate variability is principally related to the degree of left ventricular impairment and is independent of aetiology and the presence of ventricular arrhythmias. The data suggest that analysis of heart rate variability does not help the identification of patients with congestive heart failure at increased risk of sudden death.

Adult↗
PubMed1999

Relation of mean heart rate and heart rate variability in patients with left ventricular dysfunction.

The new finding was that mean heart rate and heart rate variability were more closely coupled in patients with more advanced LV dysfunction. Mean heart rate explained a larger portion of variance in heart rate variability in patients in the lowest LVEF quartile than in those in the highest one. These results support our hypothesis that sympathetic activation in patients with more severe LV dysfunction results in closer correlation between heart rate and heart rate variability. Generally, the correlation between mean heart rate and heart rate variability is weak because heart rate and heart rate variability represent different modalities of cardiovascular regulation. Mean heart rate is normally determined by the interactions of both the sympathetic and parasympathetic nervous systems, whereas modulation of these activities, with different gains, determines the magnitude of heart rate variability. This results in great complexity in control of the heart by the autonomic nervous system. However, heart rate is likely to be more dominantly regulated by the sympathetic nervous system because of vagal withdrawal in patients with more severe LV dysfunction. The effect of sympathetic cardiac modulation has been shown to be more sluggish than that of the parasympathetic nervous system in beat-to-beat regulation of heart rate. This may result in more blunted heart rate variability concomitantly with elevated mean heart rate. Thus, variation in heart rate variability in any given mean heart rate is likely to be lower than in patients with more preserved LV function, and hence with more complex cardiac autonomic regulation with involvement of the parasympathetic nervous system. Indeed, even the slopes of regression lines between mean heart rate and heart rate variability were similar in the first and fourth LVEF quartile; the intercept of the regression line was significantly higher in the fourth quartile than in the first one. This further supports our hypothesis.

Adult↗
PubMed1998

[Ischemic preconditioning in the aged heart--myocardial protective effect as compared with the mature heart].

It is now well established that pre-treatment with sublethal ischemia, followed by reperfusion, will delay myocardial necrosis during a later sustained ischemic episode, termed ischemic preconditioning (IPC); this has been confirmed experimentally and clinically. However, the effects for the senescent heart differ from those of the mature heart at both functional and cellular levels which have not yet been determined. Comparisons were made between aged (> 135 weeks, n = 18) and mature (15 approximately 20 weeks, n = 8) rabbit hearts which underwent 30 min. normothermic global ischemia with 120 min reperfusion in a buffer-perfused isolated, paced heart model, and the effects of IPC on post-ischemic functional recovery and infarct size were investigated. Ischemic preconditioned hearts (n = 6) were subjected to one cycle of 5 min. global ischemia and 5 min. reperfusion prior to global ischemia. Global ischemic hearts (n = 6) were subjected to 30 min. global ischemia without intervention. Control hearts (n = 6) were subjected to perfusion without ischemia. Post-ischemic functional recovery was better in the ischemic preconditioned hearts than in the global ischemic hearts in both aged and mature hearts. However, in the aged hearts, post-ischemic functional recovery was slightly reduced compared to that of the mature hearts, and only the coronary flow was well-preserved. In the mature hearts, myocardial infarction in the ischemic preconditioned hearts (14.9 +/- 1.3%) and in the control hearts (1.0 +/- 0.3%) was significantly decreased (p < 0.01) compared to that of the global ischemic hearts (32.9 +/- 5.1%). In the aged hearts, myocardial infarction in the ischemic preconditioned hearts (18.9 +/- 2.7%) and in the control hearts (1.1 +/- 0.6%) was significantly decreased (p < 0.001) compared to that of the global ischemic hearts (37.6 +/- 3.7%). The relationship between infarct size and post-ischemic functional recovery of left ventricularpeak developed pressure (LVDP) was linear and the correlation negative, with r = -0.934 (p < 0.001) and -0.875 (p < 0.001) for mature and aged hearts respectively. The data suggest that, in the senescent myocardium, the cellular pathways involved ischemic preconditioning responses that were post-ischemic, and that functional recovery was worse as compared to that of the mature myocardium. Furthermore, the effects of post-ischemic functional recovery became consistently weaker during the control period of 120 min. reperfusion after a prolonged ischemic insult in a buffer perfused isolated rabbit model. However, the effects of infarct size limitation were well-preserved in both senescent and mature myocardia.

Aging↗
PubMed1995

Heart rate increase and maximal heart rate during exercise as predictors of cardiovascular mortality: a 16-year follow-up study of 1960 healthy men.

BACKGROUND: Resting heart rate is directly associated and maximal exercise-induced heart rate inversely associated with cardiovascular mortality, and therefore their difference might contain prognostic information from both variables. The comparative long-term prognostic values of maximal exercise-induced heart rate and of the difference between it and resting heart rate were studied in apparently healthy middle-aged men. METHODS: Resting heart rate and maximal exercise-induced heart rate were measured, and their difference calculated, in 1960 apparently healthy men aged 40-59 years, and mortality was recorded over a period of 16 years. Conventional coronary risk factors were assessed at baseline. RESULTS: Both the difference between the two heart rates and the maximal exercise-induced heart rate were strongly, independently and inversely associated with cardiovascular mortality after adjustment for age, smoking, systolic blood pressure, lung function, glucose tolerance, serum cholesterol level, serum triglycerides level, physical fitness and exercise ECG findings. The adjusted relative risk of cardiovascular death in heart-rate difference quartiles 3 and 4 compared with that in quartile 1 (the lowest heart-rate difference quartile) was 0.54 (95% confidence interval 0.33-0.86; P = 0.009). The corresponding value for maximal exercise-induced heart rate was 0.56 (95% confidence interval 0.34-0.89; P = 0.018). Within the lowest heart-rate difference quartile, but not within the lowest maximal exercise-induced heart rate quartile, a further, strong, negative gradient in cardiovascular mortality was observed. In the high working capacity range, low heart-rate difference but not low maximal exercise-induced heart rate predicted very high cardiovascular disease mortality. Heart-rate difference and maximal exercise-induced heart rate were also inversely associated with non-cardiovascular disease mortality. CONCLUSIONS: Both heart-rate difference and maximal exercise-induced heart rate were strong, graded, long-term predictors of cardiovascular mortality among apparently healthy middle-aged men, independent of age, physical fitness and conventional coronary risk factors. However, low heart-rate difference was a better predictor than low maximal exercise-induced heart rate for recognizing individuals who were at particularly high risk of dying prematurely from cardiovascular diseases.

Adult↗
PubMed2000

Importance of heart rate for acute hibernation in isolated blood-perfused piglet hearts.

BACKGROUND: Hibernating myocardium may benefit from revascularization. There are several experimental models for acute hibernation. In intact hearts low-flow ischemia causes time-dependent metabolic alterations, termed "metabolic adaptation". In isolated heart preparations metabolic responses to low-flow ischemia vary, and signs of metabolic adaptation are not consistently found. In isolated hearts global ischemia may cause bradycardia unless the hearts are paced. We hypothesized that the lack of consistent metabolic adaptation to low-flow ischemia in isolated hearts might be due to bradycardia during ischemia. In this study we investigated the influence of heart rate on metabolism and function in an isolated heart preparation. METHODS: Isolated blood-perfused piglet hearts were subjected to 120 min 10% flow. In groups A (n=9) and B (n=4) hearts were not paced during ischemia, in groups C (n=5) and D (n=5) hearts were paced at pre-ischemic heart rate during ischemia. RESULTS: Without pacing, heart rate declined to approximately 1/3 during ischemia and anaerobic metabolism showed a slight decline over time. With pacing, production of protons, pCO2 and lactate showed a bell-shaped curve which peaked at 20-25 min of ischemia, followed by a subsequent decline towards the end of ischemia (overall p < 0.001 for all). However, reperfusion revealed impaired recovery of function in paced hearts compared to non-paced hearts (53 +/- 7% vs 77 +/- 4%, p < 0.05) concomitant with higher release of creatine kinase (455 +/- 93 IU/100 g vs 106 +/- 13 IU/100 g, p < 0.01). CONCLUSIONS: When heart rate is allowed to decline during low-flow ischemia in isolated piglet hearts, signs of metabolic adaptation are not evident. When hearts are paced during ischemia time-dependent alterations in anaerobic metabolism occur, resembling observations seen in intact beating hearts. However, paced hearts also show indications of increased cellular injury, indicating that in paced hearts the metabolic consequences are mostly due to increased irreversible cell injury. Thus, the model for acute hibernation with 10% flow in isolated blood-perfused piglet hearts are critically dependent on bradycardia during ischemia.

Acute Disease↗
PubMed2006

ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death--executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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Anti-Arrhythmia Agents↗
PubMed2006

ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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Atrial Fibrillation↗
PubMed2006

ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.

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Arrhythmias, Cardiac↗