tetano
Editor, Senior Moderator
Ionnina, Greece - Electrocardiographic (ECG) anomalies frequently appear in patients with the H1N1 flu, but the pathogen does not appear to affect the heart directly, a new study shows [1].
Many pathogens are known to directly induce ECG changes, but the cardiac effects by the new H1N1 influenza strain have not been studied yet, according to Dr Nikolaos Akritidis (General Hospital, Ioannina, Greece) and colleagues. To understand the epidemiological and clinical characteristics and outcomes of ECG anomalies in H1N1 patients, the authors evaluated all patients admitted to their center with the diagnosis of novel H1N1 infection with ECG when the patient was admitted and then subsequently daily. Their results are published September 28, 2010 in the American Journal of Cardiology.
A total of 50 H1N1 patients were admitted and included in the study, of which 14 had ECG abnormalities. Those 14 were further evaluated with ultrasonography for underlying or ongoing heart disorders and serial assessments of serum cardiac troponin I and creatine kinase-MB values.
The "prominent findings" in these 14 patients were T-wave inversions and ST-segment depression, but none of the patients exhibited any increases in serum creatine kinase-MB, and serum troponin I was negative in all but one patient, who transiently exhibited upper-normal-limit troponin I levels. All of the observed ECG changes reversed during disease regression. Ultrasonography excluded the presence of pericarditis or mitral-valve prolapse, which could otherwise account for T-wave inversions, and none of the ultrasounds showed alterations in left ventricular contractility in any patient. There were no cases of bundle branch block, and serum potassium levels were normal in all patients
There were no statistically significant differences in age, gender, comorbidities, or laboratory parameters between the H1N1 patients who exhibited ECG alterations and those with normal ECGs. However, the patients with ECG changes were more likely to have lower-respiratory-tract symptoms of the H1N1 flu than patients with normal ECGs (78% vs 64%), and two patients died of respiratory failure, but there were not enough patients to show a statistically significant connection between the ECG abnormalities and lower-respiratory-tract infection.
Previous studies have shown that a flu pathogen could cause an ECG anomaly by inducing myocarditis and early myofibril necrosis leading to rapid deterioration. And a recent study in California, reported by heartwire, found several cases of myocarditis among children with H1N1. But "this was not the case in our series, in which adverse outcomes were not related to persistent cardiac or ECG abnormalities, being principally a consequence of severe respiratory involvement."
These ECG changes accompanying acute novel H1N1 infection "may depict systemic alterations of acute infection," Akritidis et al explain. "The alterations observed in our series may also reflect transient ischemia or the effect of systemic inflammatory response on the myocardium. Irrespective of the pathogenetic mechanism involved, however, all changes observed were transient."
http://www.theheart.org/article/1130799.do
Many pathogens are known to directly induce ECG changes, but the cardiac effects by the new H1N1 influenza strain have not been studied yet, according to Dr Nikolaos Akritidis (General Hospital, Ioannina, Greece) and colleagues. To understand the epidemiological and clinical characteristics and outcomes of ECG anomalies in H1N1 patients, the authors evaluated all patients admitted to their center with the diagnosis of novel H1N1 infection with ECG when the patient was admitted and then subsequently daily. Their results are published September 28, 2010 in the American Journal of Cardiology.
A total of 50 H1N1 patients were admitted and included in the study, of which 14 had ECG abnormalities. Those 14 were further evaluated with ultrasonography for underlying or ongoing heart disorders and serial assessments of serum cardiac troponin I and creatine kinase-MB values.
The "prominent findings" in these 14 patients were T-wave inversions and ST-segment depression, but none of the patients exhibited any increases in serum creatine kinase-MB, and serum troponin I was negative in all but one patient, who transiently exhibited upper-normal-limit troponin I levels. All of the observed ECG changes reversed during disease regression. Ultrasonography excluded the presence of pericarditis or mitral-valve prolapse, which could otherwise account for T-wave inversions, and none of the ultrasounds showed alterations in left ventricular contractility in any patient. There were no cases of bundle branch block, and serum potassium levels were normal in all patients
There were no statistically significant differences in age, gender, comorbidities, or laboratory parameters between the H1N1 patients who exhibited ECG alterations and those with normal ECGs. However, the patients with ECG changes were more likely to have lower-respiratory-tract symptoms of the H1N1 flu than patients with normal ECGs (78% vs 64%), and two patients died of respiratory failure, but there were not enough patients to show a statistically significant connection between the ECG abnormalities and lower-respiratory-tract infection.
Previous studies have shown that a flu pathogen could cause an ECG anomaly by inducing myocarditis and early myofibril necrosis leading to rapid deterioration. And a recent study in California, reported by heartwire, found several cases of myocarditis among children with H1N1. But "this was not the case in our series, in which adverse outcomes were not related to persistent cardiac or ECG abnormalities, being principally a consequence of severe respiratory involvement."
These ECG changes accompanying acute novel H1N1 infection "may depict systemic alterations of acute infection," Akritidis et al explain. "The alterations observed in our series may also reflect transient ischemia or the effect of systemic inflammatory response on the myocardium. Irrespective of the pathogenetic mechanism involved, however, all changes observed were transient."
http://www.theheart.org/article/1130799.do