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PubMed1992

[Diagnosis and therapy of post-infarction cardiac complications].

The authors discuss the diagnosis and treatment of acute myocardial infarct complications. They describe a rare combination of these complications: interventricular septum rupture and left ventricular aneurysm with envelope perforation, filled by a thrombus.

Female↗
PubMed1992

[Clinical case and review of the subject. Prognosis in acute myocardial infarction].

Aiming to discuss the value of the prognostic indices in the acute myocardial infarction (AMI), we present two cases of AMI, where the predictable prognosis at 48 hours of the onset of symptoms is informed by the outcome of each case. In the first one, a patient in cardiogenic shock had a good evolution because he suffered a biventricular infarction that responsed well to hydric overcharge. The other case, a Killip classe I infarction, was complicated by a late left ventricular free wall rupture. We discuss the several aspects of each case, and finally we do a critical aproach of the most common prognostic indices (Killip and Kimbal classes, Peel prognostic groups and Norris prognostic groups).

Heart Rupture, Post-Infarction↗
PubMedDate not supplied

Transcatheter closure of ventricular septal defect: a nonsurgical approach to the care of the patient with acute ventricular septal rupture.

Acute ventricular septal rupture is a potentially fatal complication of myocardial infarction. In the past, surgical repair was the only treatment option for this life-threatening event. However, not all patients are good surgical candidates. Transcatheter closure of a ventricular septal defect (VSD) with a prosthesis called the Rashkind Patent Ductus Arteriosis Occluder System allows closure of the VSD without the possible complications associated with open-heart surgery. This treatment has potential as a temporary measure for patients awaiting surgical repair of VSD. Transcatheter closure may also be used as a permanent treatment for those patients considered to be poor surgical candidates. This case presentation addresses the use of a state-of-the-art nonsurgical approach to VSD closure. The focus is on the unique medical and nursing interventions used in caring for the patient suffering from a myocardial infarction complicated with postinfarction ventricular septal defect.

Aged↗
PubMed1992

Postinfarction cardiac rupture in the nineties: do we know determinating factors?

Postinfarction cardiac rupture (PCR) up to the present accounts for approximately 20 percent of autopsy infarcted cases, ranking only behind arrhythmias and cardiac failure in the frequency of AMI complications. We re-examined our observations of a previous anatomo-clinical study of 96 patients who underwent autopsy after death from AMI. Sixteen patients had rupture of the free wall of the left ventricle at the site of infarction. All the patients with rupture showed the following statistically significant characteristics (p less than 0.01) if compared to those without rupture: cardiac hypertrophy (heart weight 390 to 1020 gm; mean: 627.5 +/- 201 gm; left ventricular wall thickness 18 mm to 29 mm; mean: 25.17 +/- 3.6 mm), sudden death (6 cases) without premonitory symptoms or with symptoms of less than an hour's duration or reappearance of chest pain not improved by opiates before late death, that occurred 240 to 660 minutes from chest pain, recorded electrocardiograms showing sinus rhythm with unchanged ST-segment (12 cases), atrioventricular block (2 cases) and junctional rhythm (2 cases). Hypertension pre-existing to the infarction was seen in 6 cases with rupture versus 9 cases without rupture (p less than 0.01). Blood pressure, heart weight and wall thickness of the left ventricle are the most increased parameters in the patients with PCR. Preventive measures against these factors can reduce PCR.

Aged↗
PubMed1992

[Cardiac rupture and tamponade in a pregnant woman with acute myocardial infarction].

A case is described of a 35-year old pregnant woman (38-th week, tertigravida) with an acute myocardial infarction (AMI). The diagnosis of anterolateral myocardial infarction was based on the clinical, biochemical, ecg and echocardiographical findings. Ventricular premature beats were observed in the tenth day of AMI: Delivery was accomplished by cesarean section without complications. In the second day after the cesarean section the patient died. On autopsy cardiac rupture, tamponade and fresh necrosis of the lateral wall was found.

Adult↗
PubMed1991

[Sudden death in acute myocardial infarct in hospitalized patients: a clinical and anatomicopathological study over a 10.5-year period].

The paper reports on the study of 1457 patients with acute myocardial infarct (Ami) admitted in the word of the cardiac intensive care of the clinic for 10.5 years. The general mortality was of 21.2% and the sudden death (defined as such when appeared suddenly within less than 1 hour from the onset of the acute symptoms, but after 24 hours from the onset of AMI in a patient apparently equilibrated) appeared in 114 patients who were examined postmortem (43.3% of the total of the deaths). The main causes of the SD was rupture of the myocardium (28.8% of the general mortality), primary ventricular fibrillation (22.0%) and thromboembolic phenomena (17.8%). The sudden death by rupture of the myocardium appeared in a first AMI, usually large and was not helped by the anticoagulant treatment or by other therapy. Primary ventricular fibrillation appeared during the first week from the onset and was favoured by the ventricular hyperexcitability and active myocardial ischemia (which were not specific). Xyline (only more than 2 mg/min) and amiodarone gave a good protection. The sudden death by systemic thromboembolization appeared almost only in the antero-lateral myocardial infarcts, 5-8 days after the onset. The appearance of a small flow syndrome "sine materia" with or without association of some recurrent arrhythmias was suggested. Efficient anticoagulation prevented systemic thromboembolization and, to a smaller extent to pulmonary thromboembolization.

Cause of Death↗
PubMed1991

Surgical treatment of acute myocardial infarction.

In recent years, advances in surgical techniques and perioperative management of cardiac surgical patients have facilitated more aggressive operative treatment of many serious and even catastrophic complications of acute myocardial infarction (MI). In addition, improved understanding of the natural history of these complications has helped to optimize the indications for and timing of surgical intervention. The role of emergency revascularization for postinfarction angina, evolving acute MI, cardiogenic shock after acute MI, and failed percutaneous transluminal angioplasty has expanded with overall satisfactory to excellent results. Surgical treatment of mechanical with overall satisfactory to excellent results. Surgical treatment of mechanical complications of acute MI such as free-wall rupture, acute ischemic mitral insufficiency, and ventricular septal defect also is undertaken earlier and more aggressively. Although the mortality rates for these conditions remain higher than desired, salvage of many previously doomed patients now is a reality.

Acute Disease↗
PubMed1991

Complicated acute myocardial infarction. Heart failure, shock, mechanical complications.

In-hospital mortality in patients with acute myocardial infarction is predominantly related to heart failure or shock and mechanical complications (acute mitral regurgitation, ventricular septal rupture, and free wall rupture). Heart failure and shock are primarily the consequences of contractile dysfunction of the left ventricle. Use of inotropic agents and assist devices are temporizing measures; early reperfusion with salvage of ischemic interventricular septum or free wall, resulting in severe mitral insufficiency, left to right shunt, and acute tamponade, respectively, necessitates immediate diagnosis and surgical intervention.

Acute Disease↗
PubMedDate not supplied

Apparent rupture of the ventricular septum after myocardial infarction in an infant with congenital heart disease.

Clinical and angiocardiographic simulation of rupture of the interventricular septum, in an infant with an endocardial cushion defect and documented myocardial infarction is reported. Close straddling of a proven congenital muscular apical ventricular septal defect by trabeculae carne is believed to have led to the angiocardiographic simulation of a post-infarction apical ventricular septal defect. In the surgical approach to post-infarction ventricular septal defects, the implication of such a simulation could be important.

Heart Rupture↗
PubMed1979

[Surgery of ventricular aneurysms and akinetic zones].

Operation was performed in 180 patients with post-infarction ventricular aneurysm (12 cases) or akinesia (92 cases). Simultaneously in 2 cases mitral valve replacement was performed and in 2 cases ruptured ventricular septum was treated by patch. The results are reported and discussed.

Adult↗
PubMed1979

[False aneurysm associated with mitral insufficiency due to rupture of the heart at the point of insertion of the anterior papillary muscle. A successfully operated case].

Although rupture of a mitral papillary muscle during myocardial infarction is well known, and post-infarction transmural ruptures causing false aneurysms occasionally reported, the association of rupture of the anterior papillary muscle and a underlying transmural parietal rupture giving rise to a false aneurysm is quite exceptional, and, to the best of our knowledge, has not previously been reported. Despite the serious nature of the disease, surgical cure of the aneurysm with mitral valve replacement was successful, due to the limitation of the anatomical disruption by early pericardial symphysis.

Aneurysm↗
PubMed1976

Post-infarction cardiac rupture.

Three allied conditions are described in this paper: (i) haemopericardium with cardiac rupture (5 cases); (ii) haemopericardium without rupture (2 cases); (iii) pseudoaneurysm (1 case). In the first 2 of these, the significant features were clinical deterioration with shock 3 or more days after infarction, recurrent cardiac pain, cardiac tamponade, and immediate or later ineffectiveness of counterpulsation. An additional feature in the second group was the development of haemopericardium after heparin therapy. In the third group, infarction followed by left ventricular failure and progressive cardiac enlargement was the significant feature. An apical systolic murmur was not present, as a false sac had not been formed. Ante-mortem diagnosis depends upon an appreciation of these features. Without it successful surgery is impossible. There were 4 survivors in this group of 8 patients.

Aged↗