High Wall Motion Score Index after Acute Myocardial Infarction is Associated with Worse In-Hospital Outcome.

Myocardial Infarction is a major cause of death and disability worldwide. The incidence of coronary heart disease is high and second most cause of death after cancer. This prospective study conducted on 100 patients admitted with first attack of acute myocardial infarction in the department of Cardiology in Mymensingh Medical College Hospital, Mymensingh, Bangladesh from July 2012 to June 2013 who were observed 3 to 8 days of hospital stay without doing further echocardiography and evaluated the relationship between echocardiographic wall motion score index (WMSI) assessed within 24 hours of admission and in-hospital outcomes. Mean age was 53.24±10.17 years in WMSI <2 and 55.58±12.68 years in WMSI ≥2 groups; difference was statistically non-significant (p>0.05). In both groups, males were predominant sufferer. Male-female ratio was 3.55:1 and the difference was statistically non-significant (p>0.05). As a risk factor, smoking was significantly higher in both groups but the difference was not statistically significant (p>0.05) between groups. Hypertension was 34(49.28%) cases in WMSI <2 and 13(41.93%) cases in WMSI ≥2 group; difference was not statistically significant (p>0.05). Diabetes mellitus was 13(18.84%) cases in WMSI <2 and 16(51.61%) cases in WMSI ≥2 group that was statistically significant (p<0.05). Dyslipidemia was 28(40.58%) cases in WMSI <2 group and 23(74.19%) cases in WMSI ≥2 group that was statistically significant (p<0.05). Site of involvement of MI in WMSI <2 group were 39(56.52%) cases AMI (Anterior) and 30(43.48%) cases AMI (Inferior). In WMSI ≥2 group, AMI (Anterior) were 29(93.55%) and AMI (Inferior) were 02(6.45%). It revealed that AMI (anterior) was significantly higher in WMSI ≥2 group and AMI (Inferior) was significantly higher in WMSI <2 group. Heart failure class (Killip class) increases with the increasing of WMSI. In Killip class-I, 4(5.80%) were WMSI <2 and 01(3.23%) was WMSI ≥2 (p>0.05). In Killip class-II, 8(11.59%) were WMSI <2 and 02(6.45%) were WMSI ≥2 (p>0.05). In Killip class-III, 4(5.80%) were WMSI <2 and 13(41.94%) were WMSI ≥2 (p<0.05). In Killip class-IV, 2(2.89%) were WMSI <2 and 05(16.13%) were WMSI ≥2 (p<0.05) that was statistically significant. Arrhythmia was 14(20.29%) cases in WMSI <2 group and 13(41.94%) cases in WMSI ≥2 group that was statistically significant (p<0.05). Death was 2(2.90%) cases in WMSI <2 and 07(22.58%) cases in WMSI ≥2 group that was statistically significant (p<0.05). Early mortality rate was greater in patients with both WMSI ≥2 and a higher Killip's class. The higher the WMSI determined within 24 hours of admission, the worse the in-hospital outcome. Echocardiography is an affordable and readily available technique, which may be used to identify and stratify the risk following acute MI.

[Partial pericardium defect with a cardiac heart diverticulum and extensive intrauterine hypoxic myocardial lesions]. / Partieller Perikarddefekt mit herniertem Herzdivertikel und ausgedehnten intrauterinen hypoxischen Myokardschädigungen.

The autopsy of a fetus at 23 weeks gestational age revealed a partial pericardial defect with subsequent herniation of parts of the left ventricle. The myocard was impinged by the fibrous rim of the residual pericardium. Microscopic examination showed signs of recurrent myocardial infarctions with necrosis, calcification, fibrosis and prominent deposition of iron.Partial pericardial defects result from incomplete fusion of the pleuropericardial membrane and may lead to myocardial infarction via compression of the coronary arteries.

Biochemical markers of neonatal myocardial dysfunction.

INTRODUCTION: Cardiac ultrasounds (US) are not always available at the bedside. Cardiac Troponin I (cTnI), CK-MB and NT-proBNP may be an alternative or complementary to influence evaluation and treatment. OBJECTIVES: To determine reference ranges of biochemical markers cTnI, CK-MB and NT-proBNP in normal neonates. METHODOLOGY: Cord and blood samples were collected from neonates and the above biochemical markers were determined. Ultrasounds were performed blindly. RESULTS: CK-MB remains constant from cord blood to the first day, declining thereafter to almost half the values (81.5 vs 52.0 U/l); cTnI increases from 0.004 to 0.058 ng/ml by 72 h falling to 0.030 by day 10; NT-proBNP peaks by 24 h (5085.5 pg/ml), subsiding to 3388.5 pg/ml by day 3, falling to 1316.0 pg/ml by day 10. CONCLUSIONS: CK-MB, mostly of muscle origin and reflecting labor stress or injury, is not to recommend as a measure of myocardial damage in the neonate. The rise in cTnI may be explained by a degree of myocardial involvement, albeit physiological. The initial rise and subsequent fall of NT-proBNP represents the physiological ventricular overload of transient birth adaptation.

Myocardial infarction in a neonate with left-sided congenital diaphragmatic hernia.

We present a case study of a newborn girl with a left-sided congenital diaphragmatic hernia and a myocardial infarction (MI). The occurrence of MI in newborns has been associated with cardiac malformations and abnormalities of the coronary arteries or thromboembolization. In our patient, echocardiography revealed left ventricular dysfunction, persistent pulmonary hypertension and an inferolateral MI. Within 24 hours cardiac function and oxygenation did not improve and the baby died. Autopsy showed massive MI, a small aortic valve and ascending aorta, and hypoplasia of the distal aortic arch and isthmus. An accessory spleen was also present. The present report underlines the importance of cardiac evaluation in patients with congenital diaphragmatic hernia.

[Levosimendan-long-term inodilation in an infant with myocardial infarction]. / Säugling mit therapie-refraktärer suprasystemischer pulmonaler Hypertonie nach MyokardinfarktIntermittierende Stabilisierung mit Levosimendan, einem neuartigen Langzeit-Inodilatator.

An infant with myocardial infarction due to congenital stenosis of the left coronary artery with consecutive left ventricular dysfunction and mitral regurgitation developed refractory pulmonary hypertension (PHT) and recurrent PHT crises. Catecholamines to support cardiac function, or pulmonary vasodilators like inhaled nitric oxide showed no effect. Treatment with Levosimendan (Simdax), a new inodilator, combining both inotropic and pulmonary vasodilating effects, improved left ventricular dysfunction, increased cardiac index, decreased pulmonary vascular resistance and reduced frequency and extent of the PHT crises. This case may suggest the use of Levosimendan as a long-term inotropic agent and pulmonary vasodilator in children with depressed cardiac function.

Significance of a Q wave in lead I in the newborn.

We present 11 healthy newborns whose electrocardiograms had a pure Q wave in lead I and who did not have a myocardial infarction clinically. We propose that in the healthy newborn, a pure Q wave in lead I may be due to increased right ventricular mass, not myocardial infarction.

Genetic polymorphism of 5,10-MTHFR reductase gene in offspring of patients with myocardial infarction.

A family history of myocardial infarction is a major determinant of ischemic disease. A C->T677 polymorphism in the methylenetetrahydrofolate reductase (MTHFR) gene has been identified as a cause of mild hyperhomocysteinemia, a risk factor for arterial thrombosis. We have investigated the relationship between the MTHFR TT genotype and a family history of myocardial infarction in a cohort of 982 apparently healthy individuals. Subjects whose first-degree relatives suffered from a myocardial infarction, showed raised median age (p <0.001), total cholesterol (p <0.001) and plasma fibrinogen (p = 0.023) and a higher than normal frequency of C-reactive protein levels >0.33 mg/dl (p = 0.012). Moreover, when compared to subjects without such family history, a higher number of homozygotes for the T allele of the MTHFR gene (p = 0.027), and of the 4G allele of the plasminogen activator inhibitor-1 gene (p = 0.002) was found in the subsetting of the offspring of patients with myocardial infarction. In a multiple logistic regression analysis, age (OR 1.02 [95%-CI: 1.00-1.05]), total cholesterol (OR 1.40 [95%-CI: 1.14-1.71]), C-reactive protein levels >0.33 mg/l (OR: 1.87 [95%-CI: 1.10-3.20]), plasminogen activator inhibitor-1 4G/4G (OR: 1.84 [95%-CI: 1.27-2.66]), and MTHFR TT genotype (OR 1.62 [95%-CI: 1.08-2.42]), were all associated with a family history of myocardial infarction. Thus, the MTHFR TT genotype independently accounts for the risk of a family history for myocardial infarction in the present setting.

Ruptura de miocardio postinfarto: estudio neocrópsico / Myocardial postinfarction rupture: neocropsico study

La ruptura de la pared ventricular como complicación de un infarto de miocardio (IAM) es rara, pero de gran letalidad. Solamente el diagnóstico temprano y la cirugía expedita pueden salvar al paciente. En el Hospital México desde 1982 a 1997 un total de 9 pacientes se mostró en la autopsia la presencia de ruptura miocárdica. Es posible que otros individuos hayan muerto por esta catástrofe ya que el número de autopsias han disminuido considerablemente. Los objetivos principales de este estudio son: a. Llamar la atención al cuerpo médico sobre esta complicación tan severa, b. Definir el perfil clínico del paciente en riesgo y c. Recomendar un plan de manejo

Dilatation of the left ventricle in a newborn: probable in utero myocardial infarction.

A case study is presented of a premature infant delivered at 32 weeks' gestation by cesarean section. At birth the infant had massive cardiomegaly with extreme left ventricular dilatation as well as severe congestive heart failure and respiratory distress. The findings at autopsy suggest that the cardiac dysfunction was secondary to a myocardial infarct occurring in utero.

[Myocardial infarct in a newborn infant]. / Myocardinfarct bij een pasgeborene.

Myocardial infarction is rarely described in the newborn. We report a case in which the newborn had a normal heart and probably normal coronary arteries. The only presenting sign was transient extrasystolic beats. The course was uneventful and our patient recovered spontaneously. A review of the literature is presented.