The Swan-Ganz catheter in myocardial infarction.
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Severe chronic rheumatoid arthritis is sometimes associated with several internal organic lesions. This is the report of a patient with malignant chronic rheumatoid arthritis complicated by an acute myocardial infarction, left ventricular wall rupture and pseudoaneurysm besides reactive amyloidosis and perimyocarditis.
OBJECTIVE: To evaluate age group and i.v. thrombolytic therapy (TT) influences on cardiac rupture complicating acute myocardial infarction (AMI). CONCEPTION: Retrospective analysis of patients (pts) admitted during 1988-89 to an Intensive Care Unit of a Terciary Hospital (UCIM) with AMI. POPULATION: 430 pts were admitted with AMI. During this period 89 pts were submitted to TT (25% age greater than or equal to 65 years). Eighty four pts died during hospital stay and 42 had autopsy study (50%). Only 7 of nonautopsied pts died of undetermined cause. Dead pts had age m +/- SD 72 +/- 11 years old (yo) (37% female, 63% male and 74% age greater than or equal to 65 yo). RESULTS: Nineteen pts died of cardiac rupture (CR) (23%). CR prevalence was 1.4% (3/218) in pts less than 65 yo and 7.5% (16/212) in pts greater than or equal to 65 yo (p less than 0.01). CR prevalence in pts submitted to TT (4.5%) 4/89, was similar to pts not submitted to TT (4.4%) 15/341 (n.s.). Pts less than 65 yo had nonsignificant differences in CR wether submitted or not to TT (0% vs 2%). Elderly pts (greater than or equal to 65 yo) CR prevalence was 18% (4/22) in those submitted to TT vs 6% (12/190) in those not submitted to TT (p less than 0.05). CONCLUSIONS: Thrombolytic therapy may carry an additional risk for cardiac rupture in elderly patients (greater than or equal to 65 yo).
The authors report two cases of cardiac rupture during acute myocardial infarction successfully treated surgically. In the first case, rupture occurred 7 days after hospital admission for anteroseptal myocardial infarction. The patient developed sudden cardiogenic shock with signs of venous hypertension without left ventricular failure. The second patient was admitted for syncopal chest pain with transient hypotension which regressed after volume repletion and pressor amine therapy. On admission, the patient had signs of cardiac tamponade. The ECG showed recent inferolaterobasal myocardial infarction. In both cases the diagnosis was made by 2D echocardiography which showed voluminous circumferential pericardial effusions probably due to haemorrage, with an image very suggestive of a blood clot in the effusion of the second patient. The two patients underwent emergency cardiac surgery and both survived with a 4 and 1.5 month follow-up respectively. These two cases confirm the value of 2D echocardiography as an emergency bedside procedure for the diagnosis of cardiac rupture, especially when images of intrapericardial thrombosis are observed, as in our second patient. In addition, the first case raises once again the question of the role of late thrombolysis as a predisposing factor of cardiac rupture at a time when this technique is proposed up to 24 hours after the onset of symptoms.
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Forty one cardiac rupture complicating acute myocardial infarction (AMI) were studied in a ten-year period. The anterior AMIs are most likely to be observed with ruptures. The interval from the onset of AMI to the clinical detection of rupture was short (acute period). Some factors such as physical work in the acute period and transmural infarctions strongly infiltrated with leukocytes cause a higher frequency of rupture. Diabetes and hypertension might be predisposing factors.
A prospective study was done on 110 patients, 55 Chinese and 55 American elderly who had clinically proved acute myocardial infarction with histologic confirmation. The Chinese patients were much more likely to have typical pain than the American (65.4% vs 49.0%). The incidence of painlessness was only 18.1% vs 36.3%. The difference has statistical significance (P less than 0.05). Cardiac failure, shock, pulmonary infection as a major complication had no statistical significance, but the incidence of cardiac rupture group was 29.0% vs 10.9%. Ventricular fibrillation incidence was 18.1% in the Chinese vs 45.4% in the American. The incidence of recent occlusive coronary thrombi, hemorrhage and rupture of plague in coronary arteries had significant statistical difference. The incidence of triple, double and single vessel diseases were 41.8%, 29.0% and 27.2% in the Chinese group vs 36.3%, 27.2% and 25.4% in the American respectively.
The instant of cardiac rupture was initially recorded using two-dimensional echocardiography in a patient with acute myocardial infarction. This 70-year-old woman was admitted to our hospital because of chest pain lasting for six hours. The admission electrocardiogram showed Q waves and S-T segment elevations in leads I, aVL, and V4-6. Two-dimensional echocardiography revealed hypokinesis in the middle and apical portions of the anterior septum and hyperkinesis in the basal portion of the anterior septum and the posterior wall. When the patient suddenly lost consciousness, echocardiography detected a rapidly developing pericardial effusion, which filled the pericardial sac within 13 sec. A myocardial tear was recognized at the apex of the left ventricle between portions of the hypokinesis and hyperkinesis. A simultaneously-recorded electrocardiogram showed sinus rhythm (84/min) which did not change at the moment of rupture and lasted further for 15 sec until a sudden alteration to sinus bradycardia (46/min) occurred. Cardio-pulmonary resuscitation was unsuccessful and the patient died. This is the first such case in the medical literature in which the instant of cardiac rupture was recorded. Detailed reviews of the video tapes revealed that rapid accumulation of pericardial fluid occurred, followed by transient sinus bradycardia, most likely due to vagal reflex to the stretched pericardium.
Thirty-one patients underwent repair of postinfarction ventricular septal defect (VSD) from 1980 to 1989. All patients were in New York Heart Association functional class IV, and 15 of them were in cardiogenic shock when operated on. Coronary arteriography was performed in all patients before surgery: nine had one-vessel, 11 had two-vessel, and 11 had three-vessel disease. The VSD was anterior in 15 patients and posterior in 16. The operative technique evolved over the years from a fairly extensive infarctectomy and reconstruction of the septum and right and left ventricular walls with a double Dacron patch, to minimal or no infarctectomy and closure of the VSD by excluding the infarcted muscle from the left ventricular cavity. This is accomplished by suturing a single patch of bovine pericardium to healthy endocardium surrounding the infarcted muscle. The right ventricle is left intact. Overall mortality was 10%, with three operative deaths. All deaths occurred in patients in cardiogenic shock who had three-vessel coronary artery disease. Thus, the mortality for patients in shock was 20%, and the mortality for patients with three-vessel disease was 27%. The operative mortality for patients with posterior VSD was twice as high as in patients with anterior VSD. However, univariate analysis of various clinical, hemodynamic, and operative variables indicated that only three-vessel disease was predictive of operative mortality. Because the number of patients was small and the overall operative mortality relatively low, the results of this analysis may not be valid.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac tamponade during acute myocardial infarction is a life-threatening complication that can be confounded with right ventricular infarction. The most frequent cause of this complication is cardiac rupture. We report here a patient with acute myocardial infarction that developed cardiac tamponade on day 7, after receiving late systemic thrombolysis. The diagnosis was suspected with echocardiography and confirmed with hemodynamic measurements. The tamponade was partially relieved with pericardiocentesis but afterwards required emergency surgery. No cardiac rupture was found but an hemorrhagic infarction. We conclude that in this case the hemorrhagic tamponade was probably related both to late thrombolysis and to post infarction pericarditis.
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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.
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.
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.