case series Management and Prognosis of Post-Myocardial Infarction Ventricular Septal Defect: A Case Series.
Salim Arous*, Anass Maaroufi, Mohamed El Ghali Benouna, Rachida Habbal
Department of Cardiology, Ibn Rush d University Hospital, Morocco.
*Corresponding author: Salim Arous, Department of Cardiology, Ibn Rushd University Hospital, Morocco.
Received Date: 09 February 2023
Accepted Date: 13 February 2023
Published Date: 15 February 2023
Citation: Arous S, Maaroufi A, Benouna MEG, Habbal R (2023) Management and Prognosis of Post- Myocardial Infarction Ventricular Septal Defect: A Case Series. Ann Case Report 7: 1170. DOI: https://doi.org/10.29011/2574-7754.101170
Abstract
Background: The mortality rate of ventricular septal defect post-myocardial infarction remains considerable, even if the mortality of acute myocardial infarction is decreasing in the recent decades. Ischemic ventricular septal defect is responsible for a considerable number of deaths in the immediate aftermath of a myocardial infarction.
Cases presentation: We will illustrate this deadly complication of myocardial infarction through tree cases. Their treatment was difficult and the prognosis was bad, two out of three patients died.
Conclusion: the choice of the means of closing the ventricular septal defect and the delay remains very difficult. Even if surgical repair techniques have evolved over time, the prognosis still very poor.
Keywords: Myocardial Infarction, Ventricular Septal Defect, Prognosis.
Introduction
Ventricular septal defect in acute Myocardial Infarction (MI) is a rare but lethal complication, with a very high mortality rate (97% at 30 days of MI) [1]. It is the most common mechanical complication of myocardial infarction and usually occurs in the following week [2]. The diagnosis is made by echocardiography and the First-line treatment remains surgical. The choice of the surgical repair technique depends on the seat and the size of the septal rupture. Through the observation of three patients admitted for myocardial infarction in different localities and all complicated by septal rupture; we will focus on this entity, which remains fatal until today.
Case presentation
Case 1
We report the case of a 58-year-old man, chronic smoker and diabetic, admitted for an inferior myocardial infarction non-revascularized.
The patient had a pain of epigastric region for 11 days, associated with a dyspnea class IV of the NYHA.
Clinical examination showed regular pulse at 128 bpm at rest, a blood pressure at 130/80 mmHg, cracking rales in killip II with distention of jugular veins. The cardiac auscultation revealed the presence of a pan systolic murmur along the left sternal border of 4/6 intensity.
The electrocardiogram showed sinus tachycardia with Q waves in the inferior territory. The Echocardiography demonstrated a 29-30 mm high posterior muscular septal defect (Figures 1, 2), partially clogged by trabeculations of the right ventricle with a longitudinal septal dissection and a gradient at 44 mmHg. The left ventricle was not dilated, not hypertrophied, with a discrete apical hypokinesia (EF = 68%), the right ventricle was dilated with systolic dysfunction. The pulmonary artery pression was at 86 mmHg.
Figure 1: The echocardiographic aspect of the interventricular communication.
Figure 2: The aspect of the interventricular communication flow.
The coronary angiography showed significant stenosis of the middle anterior interventricular artery, the first marginal, and an occlusion of the right middle coronary artery with a thrombotic aspect (Figures 3, 4). After stabilization by medical treatment, the patient benefited from a Coronary aortic bypass with surgical closure of his ventricular septal defect. At the 7th day of post-operative, the patient died by a septic shock due to pneumonia.
Figure 3: Significant stenosis of the middle of the anterior interventricular artery.
Figure 4: Thrombotic occlusion of the right middle coronary
Case 2
A 55-year-old man, hypertensive and diabetic for 10 years under oral antidiabetic, hospitalized for a myocardial infarction in antero-septo apical and inferior territory (Figure 5). Upon admission, the patient reports anginal pain that has been evolving for 4 days, as well as crescendo dyspnea.
Figure 5: electrocardiogram of patient number 2.
His blood pressure was 120/70 mmHg, his heart rate was 110 bpm. Cardiopulmonary auscultation revealed a left para-sternal systolic murmur associated with crackles at the pulmonary bases. There was no sign of right heart failure.
His echocardiography showed an apical muscular septal defect of 23 mm with left-to-right shunting and a gradient at 90 mmHg (Figure 6, 7, 8) with systolic pulmonary artery pressure at 30mmHg, associated with hypokinesia of the anterior, antero-septal and anterolateral walls with a large apical akinesia and a left ejection fraction at 40%. The right ventricle was not dilated with a good systolic function.
Figure 6, 7: The echocardiographic aspect of the interventricular communication.
Figure 8: The aspect of the interventricular communication flow
Coronary angiography showed an occlusion of the mean anterior interventricular artery without a collateral circulation, a non-significant lesion of the first marginal and an occlusion of the right middle coronary artery (Figure 9, 10, 11).
Figure 9, 10: occlusion of anterior interventricular artery
Figure 11: occlusion of the right middle coronary artery
The decision of the heart team was to monitor the patient for 3 weeks before proposing surgery, but the evolution was marked by the occurrence of cardiogenic shock in the third week of hospitalization and the patient died.
Case 3
A 61 year-old man, chronic smoker, admitted for an anterior myocardial infarction. The patient reports a chest pain for 6 days associated with exacerbating exercise dyspnea becoming at rest.
The clinical examination found a blood pressure at 90/70 mmHg, a heart rate at 114 bpm, a left parasternal systolic murmur with crackles at the pulmonary bases on auscultation, with distension of jugular veins.
The electrocardiogram showed Q waves in anterior and inferior territory (Figure 12).
Figure 12: electrocardiogram with Q waves in anterior and inferior territory
Trans-thoracic echocardiography shows segmental kinetic abnormalities in the anterior, antero-septal and anterolateral walls as well as an apical muscular interventricular communication of 9 mm with left-to-right shunting, a trans-septal defect gradient at 35 mmHg and pulmonary hypertension at 55 mmHg. The ejection fraction was at 30% (Figures 13, 14). The right ventricle was of normal size with a mild systolic dysfunction.
