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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen term newborn infants have been recognized as having transient tricuspid insufficiency associated with significant perinatal stress. Five of these infants underwent cardiac catheterization for presumed congenital heart disease, but had only massive tricuspid valve insufficiency. The other nine infants were diagnosed on the basis of a murmur characteristic of tricuspid valve insufficiency and on other clinical grounds. All had a history of significant perinatal stress in the form of asphyxia with or without hypoglycemia. Frequently, congestive heart failure, persistent cyanosis, and ECG evidence of myocardial ischemia were present. Twelve of the 14 survived, and in each of them all cardiac signs and symptoms, including the murmur, spontaneously resolved. The two patients who died had histopathologic evidence of necrosis in the anterior papillary muscle of the tricuspid valve. The constant features of perinatal stress, ST-T wave abnormalities on the ECG, and spontaneous resolution of the transient tricuspid insufficiency strongly suggest that this syndrome is secondary to a reversible form of myocardial dysfunction, perhaps by affecting papillary muscle specifically. We believe that hypoxia with or without hypoglycemia precipitates the events leading to this clinical syndrome which is distinguishable from other cardiac abnormalities in the newborn by the history, distinctive murmur, and the ECG abnormalities.
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PMID:Transient tricuspid insufficiency of the newborn: a form of myocardial dysfunction in stressed newborns. 13 40

In order to investigate the basis of ventricular dysfunction in patients with univentricular heart, cineangiograms of 20 patients aged between 3 weeks and 22 years were digitized frame by frame and compared with left ventriculograms of patients with other cardiac malformations. Ejection fraction was at least normal (58% to 95%) and peak rate of systolic minor axis shortening was normal in all. However in only 3 patients was the change in volume achieved by virtue of the normal change in cavity shape; in 17 the end-systolic outline was abnormally circular and shape index, 4 pi (area)/(perimeter)2, changed by less than normal (p less than 0.01). In addition, abnormalities of regional wall movement were found in 12 patients. 11 showed a consistent pattern, unlike that found in ischaemic heart disease or other congenital lesions, of delayed systolic inward movement of the antero-apical wall, associated in 9 with hypokinesis. Four of these showed secondary delay of relaxation in the same region. One patient had an isolated abnormality of isovolumic relaxation. These findings were independent of age, volume overload or degree of cyanosis, but were more common in patients with absent atrioventricular connexion. We conclude that the architectural abnormalities in univentricular hearts lead to disturbances of myocardial function which particularly affect the apex. These are detectable from an early age.
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PMID:Abnormal ventricular function in patients with univentricular heart. Cineangiographic study. 44 86

A 54-year-old housewife with pulmonary atresia and ventricular septal defect developed increasing cyanosis, dyspnea, weakness, and myocardial ischemia. Initial cardiac catheterizations with angiography, including subtraction techniques, did not definitely indicate main pulmonary artery or right or left pulmonary arteries that would make her amenable to currently available surgical correction. Single-crystal suprasternal notch echocardiography indicated the presence of a small but definite right pulmonary artery. She subsequently underwent first-stage surgical correction after angiography and selective catheterization of aortopulmonary shunt vessels, which also revealed the presence of small proximal pulmonary arteries.
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PMID:Pulmonary atresia and suprasternal echocardiography. 49 61

We conducted a retrospective analysis on 311 patients with clinical diagnosis of pulmonary embolism (PE) in a period of 3 years. 163 patients were excluded based on clinical-laboratorial criteria. The remaining 146 patients had a median age of 69 years (range: 30-91 years). 54% of the patients were male. We found dyspnea (94%), abnormal cardiopulmonary observation (89%), risk factors for venous thromboembolism (74%), tachycardia (53%), cyanosis (49%), and neck vein distension (45%) to be the most frequent findings. 64% of the patients had heart failure, 32% had myocardial ischemia, 13% had cancer, and 11% had myocardial infarction. Lactic dehydrogenase (LDH) was higher than two-fold in 54% of the patients. There was severe hypoxemia in 55% of the cases and hypocapnia in 43% of the cases. Creatinine phosphokinase (CPK) was elevated in 16% of the cases. Electrocardiography was suggestive of PE in 37% of the cases. Echocardiography showed right heart dysfunction in 30% of the cases, 92% of the patients were treated with heparin, 37 patients (25%) died, 54% of which during the first 4 days after admittance. Trying to define an index of mortality in PE we evaluated all patients by discriminant analysis coming up with 14 items with good discriminative power. By approximation of their odds-ratios we determined how many points would correspond to each item in the total sum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pulmonary embolism--mortality risk]. 147 67

Anatomical repair of transposition of the great arteries (TGA) seems more attractive than the more conventional atrial baffle procedures because of resultant left ventricular-aortic continuity. The results of anatomical repair in 16 consecutive neonates with TGA and intact ventricular septum were reviewed; special consideration was given to technique and guidelines to avoid complications. Infants underwent repair within 6 days of life (average weight, 3.3 kg). Survival was 88% (14 of 16 patients). One death occurred from pulmonary hypertension and atrial shunt reversal causing cyanosis after an uncomplicated procedure; the other was due to myocardial ischemia caused by kinking of an anomalous coronary artery after attempted repair. Complications of ventricular swelling and coronary tension or kinking were successfully treated by Silastic skin patches in 2 patients and pericardial aortic patches in 2, respectively. One patient had successful repair of supravalvular pulmonary stenosis. Because anatomical repair of TGA must be performed in the first week of life, special consideration must be given to meticulous anatomical dissection, careful coronary transfer, and optimal myocardial preservation. The excellent short-term results favor the continued application of anatomical repair of TGA with intact ventricular septum in infancy.
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PMID:Anatomical repair of transposition of the great arteries with intact ventricular septum in the neonate: guidelines to avoid complications. 355 68

Persistent fetal circulation ("PFC") is a condition characterized by perduring after birth of fetal hemodynamic pattern: persistence of high pulmonary vascular resistance then occurs. "PFC" is a high mortality syndrome recently recognized as a cause of severe cyanosis and tachypnea in full-term newborns. Perinatal hypoxia, hyperviscosity, acidosis etc, may be also responsible of a persistence of high pulmonary vascular resistance. The increased right heart pressures cause a right to left shunt across the ductus arteriosus and foramen ovale not yet completely closed at birth. In this paper the clinical and angiographic evaluation of two full-term newborns, males, 5 days and 5 months old, are described, who presented with tachypnea, cyanosis and heart failure. Moreover we want to make a critical review of medical literature about this subject. The electrocardiogram of both patients showed right ventricular hypertrophy and myocardial ischemia. The chest roentgenograms showed cardiac enlargement and increased pulmonary vascular markings. Lung and central nervous system disorders were excluded by clinical and instrumental exams. Both patients underwent cardiac catheterization and angiocardiography in order to exclude a congenital heart disease. There was just evidence of pulmonary vascular resistance and right to left shunt at ductal and atrial level. O2 100% administration in one patient determined a decrease in pulmonary resistance and the shunting abolition. Clinical and hemodynamic patterns of this syndrome are very different. There are "simple forms" with normal myocardial function and "complex" higher mortality forms with evidence of cardiac involvement. It is often difficult to distinguish such forms from the other causes of central cyanosis and/or cardiac failure in the newborn as transposition of the great arteries, total anomalous pulmonary venous connection: the individualization of the syndrome then may be impossible without cardiac catheterization. A correct diagnosis for a precocious and reasonable treatment are extremely important for the survival of such critical newborns.
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PMID:[Persistence of fetal circulation. Clinical and angiographic evaluation of two cases. Review of the literature (author's transl)]. 734 16

A 49-year-old man with ischemic heart disease attempted to commit suicide by ingesting 300 tablets (6 grams) of isosorbide dinitrate. He was admitted with shortness of breath and cyanosis. Severe methemoglobinemia was diagnosed (blood level 47 mg%). After administration of intravenous methylene blue and fluids, there was immediate improvement and he was discharged 48 hours after admission.
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PMID:[Severe methemoglobinemia following large dose of nitrate medication]. 774 49

A seventy-six-year-old man with ischemic heart disease, peripheral vascular disease, and chronic renal failure developed bilateral cyanotic toes, which upon muscle biopsy, were shown to be caused by atheromatous emboli. The probable source was atheromatosis of the abdominal aorta. The toes became gangrenous, but surgical therapy was deferred because the patient was considered a high risk. With lovastatin therapy there was complete healing and except for transient cyanosis related to temporary cessation of therapy, there has been no recurrence for the past thirty months. The possible role of lovastatin in the conservative treatment of this disorder is discussed.
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PMID:Reversal of gangrenous lesions in the blue toe syndrome with lovastatin--a case report. 821 80

Two neonates undergoing arterial switch procedure developed life-threatening pulmonary hypertension intraoperatively. In one patient, bradycardia, hypotension, and electrocardiographic (ECG) evidence of myocardial ischemia suddenly occurred 20 minutes after uneventful weaning from cardiopulmonary bypass. Lifting a palpably hypertensive main pulmonary artery (MPA) resulted in reproducible hemodynamic improvement. Because the patient was already on full ventilatory support and a nitroglycerin infusion, the MPA was suspended onto the anterior chest wall. In the other patient, after removal of intraoperative drapes, severe generalized swelling and cyanosis were noted. The central venous pressure had risen to 25 mmHg, and the PO2 had dropped to 52 mmHg on 100% FIO2. The systolic arterial pressure and ECG remained normal. Immediate reexploration revealed a palpably hypertensive MPA. The coronary arteries implanted more laterally on the neoaorta were uncompromised. Amrinone loading and infusion produced immediate improvement. We believe that surgeons should be aware that pulmonary hypertension can cause coronary artery compression and right heart failure in neonates undergoing the arterial switch procedure. Lateral placement of the coronary artery and aggressive use of pulmonary vasodilators can minimize the problem.
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PMID:Acute pulmonary hypertension complicating the arterial switch procedure. 865 18

Cardiac abnormalities in birth asphyxia were first recognised in 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the new born (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and therefore, requires treatment in the form of inotropic and ventilatory support, (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required, (v) persistent pulmonary hypertension of the new born (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory distress and cyanosis (sometimes differential). Clinical examination also reveals evidence of pulmonary arterial hypertension and right ventricular failure with systolic murmur of tricuspid and, at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.
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PMID:Cardiac abnormalities in birth asphyxia. 1112 17


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