Naslov
Unusual therapy in acute myocardial infarction

Autori
Nikolić-Heitzler, Vjeran ; Babić, Zdravko ; Bulj, Nikola ; Trbušić, Matijas ; Pintarić, Hrvoje ; Manola Šime.

Izvornik
Kardiológia (1210-0048) 14 (2005); K/C100-K/C100

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, ostalo

Ključne riječi
Acute myocardial infarction; Ventricular fibrilation; Defibrilation

Sažetak
Repeated, especially high-energy, defibrillations are the likely cause of cardiac injury and post-shock myocardial dysfunction. Potentially important pathways include production of free radicals, mitochondria dysfunction, changes in adenosine metabolism, activation of potassium ATP-channels and reperfusion injury. Current studies, based mostly on animal models, report impairment of the systolic and, especially, the diastolic function of the left ventricle which compromise resuscitability and survival. We report the case of a 61-year-old male, who was admitted to our emergency room in cardio- respiratory arrest caused by ventricular fibrillation. He was immediately resuscitated and admitted to the Coronary Care Unit, where laboratory findings, ECG and echocardiographic changes suggested acute anteroseptolateral myocardial infarction without ST elevation. The early postresuscitational period was complicated by repeated “torsade de pointes” and ventricular fibrillation. Urgent defibrillation was performed in total 71 times, despite medical treatment. Because of prolonged deep coma (Glasgow Coma Score 3) primary PCI was not performed at that time. Finally, 16 hours after arrival in hospital, improvement of the patient’s neurological condition allowed us to perform coronary angiography. An occlusion of the left anterior descending artery was established and PCI was done. After the procedure, the patient showed significant clinical and further neurological improvement, without additional ventricular arrhythmias. Renal impairment (because of high levels of CK-13000 U/l) was avoided by forced diuresis. On the 5th day after the procedure the patient developed clinical signs of heart failure, atrial fibrillation with rapid ventricular rate and ST elevation in precordial leads, but without clinical and laboratory findings of myocardial reinfarction. Neither medical nor electrical attempts (four electroshocks) of conversion proved successful. Bedside echocardiography revealed global hypokinesis, with concentric thickening, oedema and diffuse high intensity “speckling” of the myocardium and pericardial reaction. Systolic and, especially, diastolic dysfunction of the left (EFLV 40%, PHT 38 ms) and right ventricles with normal cavity dimensions were found. Acute echocardiographic changes and acute elevation of CRP, ESR, fibrinogen and BNP suggested “aseptic myo-pericarditis” as the leading process at this time. After i.v. administration of methyl-prednisolon, conversion in sinus rhythm occurred and significant clinical improvement was observed.. Control echocardiography (10th and 24th day) showed regression of myo-pericarditis and significant improvement of both systolic and diastolic function (EF LV 60%, PHT 55). Conclusion: Repeated defibrillations can lead to “aseptic myo-pericarditis” causing both systolic and diastolic dysfunction. Echocardiography plays a pivotal role in the diagnosis of this condition. Corticosteroid therapy may be of clinical benefit, despite the fact that it is counterindicated in acute myocardial infarction

Izvorni jezik
Engleski

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