Myocardial infarction complicating management of congestive heart failure in a dog

1996 ◽  
Vol 32 (1) ◽  
pp. 68-72 ◽  
Author(s):  
TC DeFrancesco ◽  
CE Atkins ◽  
BW Keene

A 7.5-kg, 10-year-old, spayed female, mixed-breed dog was evaluated for sudden onset of weakness, tachypnea, and an irregular cardiac rhythm. Congestive heart failure secondary to mitral valve regurgitation had been diagnosed six weeks earlier. The dog was stable on furosemide, enalapril, and hydralazine. Complex ventricular tachycardia, altered QRS conformation of sinus complexes, echocardiographic evidence of a hypokinetic left-ventricular free wall, and elevated creatine kinase suggested a diagnosis of myocardial infarction. Despite antiarrhythmic therapy, the dog developed ventricular fibrillation and died 36 hours after admission. Postmortem examination confirmed the myocardial infarction. Although a rare diagnosis in the veterinary patient, myocardial infarction must be considered in the differential diagnosis for sudden onset of weakness, tachypnea, and ventricular tachycardia.

2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Manuel Rodríguez Martínez ◽  
Eladio Ruiz González ◽  
Anna Parra-Llorca ◽  
Máximo Vento Torres ◽  
Marta Aguar Carrascosa

Neonatal acute myocardial infarction is an uncommon entity. We describe the case of a 4-day-old term baby who presented with respiratory distress and distal acrocyanosis. The chest radiograph demonstrated cardiomegaly without pleural effusion, and examination revealed hepatomegaly. An electrocardiogram revealed QS pattern in leads I, aVL, and V6, suggestive of ischemia. Cardiac enzymes were elevated, and echocardiogram revealed moderate left ventricular dysfunction with a thrombus at the level of the left atrial appendage. The patient required hemodynamic stabilization, vasodilatation to avoid congestive heart failure, and anticoagulation with heparin and aspirin. In the context of this unusual diagnosis, we reviewed our experience over the last 17 years as well as the existing literature on neonatal myocardial infarction.


1998 ◽  
Vol 13 (2) ◽  
pp. 68-77
Author(s):  
Simon Chakko ◽  
Raul Mitrani

This review discusses the treatment of ventricular arrhythmias and bradyarrhythmias. Recent studies addressing the management of nonsustained ventricular arrhythmias in patients with congestive heart failure and those recovering from myocardial infarction are discussed. Determination of the origin of wide QRS complex tachycardia is usually possible at the bedside and the diagnostic criteria are provided. Therapy to prevent recurrent ventricular tachycardia or ventricular fibrillation is difficult and controversial. A widely accepted approach based on electrophysiologic testing and implantable defibrillators appears to be the most effective. Recognition and management of common bradyarrhythmias including the indications for pacemakers are discussed.


1992 ◽  
Vol 262 (5) ◽  
pp. H1387-H1394 ◽  
Author(s):  
I. M. Dixon ◽  
T. Hata ◽  
N. S. Dhalla

Because Na(+)-Ca2+ exchange and Ca2+ pump are thought to play a role in sarcolemmal Ca2+ movements, we examined the Na(+)-dependent Ca(2+)-uptake and ATP-dependent Ca(2+)-uptake activities in failing heart after myocardial infarction in rats. The left coronary artery was ligated, and the viable left ventricle was used 4, 8, and 16 wk later; sham-operated animals served as controls. Increased left ventricular diastolic pressure and decreased positive and negative change in pressure over time were observed in experimental animals at 4, 8, and 16 wk; these changes were associated with accumulation of fluid in the abdominal cavity. The sarcolemmal Na(+)-dependent Ca2+ uptake was depressed in 4-, 8-, and 16-wk experimental hearts. The decrease in sarcolemmal Na(+)-dependent Ca2+ uptake in failing hearts was seen when the activity was assayed either as a function of time or Ca2+ concentration; a depression of maximal velocity without any change in activity constant for Ca2+ was observed. No alteration in the Ca2+ pump (ATP-dependent Ca2+ accumulation and Ca(2+)-stimulated adenosinetriphosphatase) activities was evident in the 4-, 8-, and 16-wk experimental groups. These data suggest that changes in the Na(+)-dependent Ca2+ handling by the sarcolemmal membrane may be associated with contractile abnormalities in this model of congestive heart failure.


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