Further information: Anatomy of the Heart (see p3) from Cardiovascular Medicine, 3rd Edn*

In order to determine whether or not new cardiomyocytes are formed during the lifetime of a human heart, this study was conducted to establish whether humans are limited to the heart muscle cells present at birth, or if cardiomyocytes are generated later in life also. Although cells in rodents have been tagged with labeled nucleotide analogs for several decades, and studies have indicated that regeneration of cardiomyocytes occurs postnatally, results have been conflicting. In humans, scientists have known that in childhood, cardiomyocytes grow bigger through a process called hypertrophy, but cells had not been observed dividing. In addition, when cardiomyocytes die as a result of a heart attack, scar tissue forms instead of heart muscle cells, and thus, the heart is weakened. Also, the proliferation that would be needed to create cardiac tumors is not usually seen. In humans, cell turnover has been difficult to study because the use of labeled nucleotide analogs, such as those used in experimental animals, cannot be used in humans due to safety concerns.

To establish the age of cardiomyocytes in humans, the authors [1] took advantage of the integration of carbon-14 into human DNA that was generated by nuclear bomb testing during the 1950s. They found that the regeneration of cardiomyocytes in humans does occur postnatally, but is insufficient to keep the heart muscle intact functionally. Cardiomyocytes renew in gradually decreasing numbers, i.e. 1% of a human’s cardiomyocytes have an annual turnover by age 25, but the number decreases to 0.45% by age 75. Fewer than 50% of cardiomyocytes are exchanged during a normal life-span. It is encouraging that cardiomyocytes have the capacity to regenerate, and it is important that researchers work to develop pharmacologic strategies to stimulate the process, thereby allowing a higher percentage of injured or dying heart muscle cells to be replaced in this manner.

[1] Bergmann O, Bhardwaj RD, Bernard S et al. Evidence for cardiomyocyte renewal in humans. Science 2009;324:98-102

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Sudden Cardiac Arrest Associated with Early Repolarization

Further information: Electrocardiography from Cardiovascular Medicine, 3rd Edn*

The authors of this study [1] examined the possibility that the electrocardiographical pattern called “early repolarization” is a marker of malignant cardiac arrhythmias. Although early repolarization is commonly considered benign, experimental studies have suggested that it has a potential relationship to sudden cardiac arrest.

In order to find substantiating clinical data to support this, data from 22 centers of 206 subjects who had been resuscitated after cardiac arrest due to idiopathic ventricular fibrillation were reviewed, and the prevalence of electrocardiographic repolarization was assessed. Early repolarization is defined by a slurring or notching that creates a positive hump, a J wave, that is found at the end of the QRS complex and the beginning of the ST segment. Idiopathic ventricular fibrillation is defined as a class of patients having no identifiable structural heart disease demonstrated by normal echocardiographic biventricular dimensions and function, no detectable coronary artery disease, and no repolarization abnormalities. The prevalence and amplitude of early repolarization was also assessed in a control group of 412 subjects from a population of health care professionals with normal echocardiographic biventricular dimensions, function, and no history of syncope.

The investigators found higher-than-expected prevalence of early repolarization in patients who had idiopathic ventricular fibrillation that caused syncope and sudden cardiac arrest (31% vs. 5%, P<0.001). Subjects with early repolarization were more likely to be male and to have a history of syncope or sudden cardiac arrest during sleep than those without early repolarization. In eight subjects, the origin of initiation of the ventricular arrhythmia was traced to a site that coordinated with the localization of repolarization abnormalities. In mean (±SD) follow-up of 61±50 months, defibrillator monitoring showed a higher incidence of recurrent ventricular fibrillation in subjects with early repolarization than in those without (hazard ratio, 2.1; 95% confidence interval, 1.2–3.5; P=0.008). These findings are of potential relevance to patients with syncope or a family history of sudden death, as early repolarization may be responsible for a portion of undiagnosed syncope or unexplained premature death.

[1] Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358:2016-23

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