Cardiac rupture in acute myocardial infarction. Various clinico-anatomical types in 42 recent cases observed over a period of 30 months

Forty two cases of complete or incomplete rupture of the free left ventricular wall were reviewed in a group of 136 patients who died of acute myocardial infarction in a Coronary Care Unit and who underwent autopsy examination over a 30 month period. Four groups were distinguished on macro and microscopic features of the rupture based on a previously defined classification established by former studies: type I rupture (13 cases) with an almost direct trajectory with little dissection and bloody infiltration of the myocardium; type II (13 cases) with a multicanalicular trajectory and widespread myocardial dissection and bloody infiltration; type III (9 cases) in which the orifice of rupture is protected by an intraventricular thrombus or a pericardial symphysis; type IV (7 cases) with incomplete epicardial, endocardial or intramyocardial rupture which never was transparietal. The clinical characteristics (age, sex, time interval before admission to the coronary care unit, previous history, ECG location of the myocardial infarcts, clinical course, Killip classification, treatment and ECG changes) and anatomical findings (weight of the heart, presence of haemopericardium, previous infarction or aneurysm, location of the infarct, presence of intraventricular thrombus or ventricular septal defect, number of vessels with over 75 p. 100 obstruction and topographical location of the rupture) were compared. The type I ruptures had smaller infarcts and a quicker terminal illness with rapid evolution to cardiac tamponade. In type II ruptures, the infarcts tended to be bigger, sometimes associated with septal rupture and the terminal illness was longer lasting than in the previous group, reflecting a longer evolution towards cardiac tamponade.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Effectiveness and limitation of the current coronary care unit in treatment of patients with complications following acute myocardial infarction

For an appraisal of effectiveness and limitation of the current coronary care unit (CCU) in treatment of patients with complications following acute myocardial infarction (MI), consecutive 557 patients hospitalized to our CCU during five years were studied. In order to assess the severity of complicating pump failure, patients were divided into four classes according to Killip's classification. Number of patients, total mortality (%) and mortality due to pump failure (%) were as follows; 333 (6%, 2%) in class I, 118 (17%, 8%) in class II, 42 (19%, 17%) in class III and 55 (84%, 80%) in class IV. Warning arrhythmias, cardiac rupture and interventricular septal perforation complicated in 184 patients, 11 and 10, respectively, and mortality due to these complications was 2%, 91% and 84% in the order. Right ventricular infarction complicated in 54 patients, but only one patient died from right heart failure. Post-MI angina manifested in 156 patients and six of them died postoperatively. Our data indicate that improvement in mortality due to pulmonary edema and arrhythmias and reduction in incidence of cardiac rupture are evident effectiveness of the CCU, and that there is no improvement in survival rate of patients with cardiogenic shock even under the use of newly introduced vasodilator and catecholamine therapy or intraaortic balloon pumping.     

A case of perforation of the interventricular septum with free wall rupture, in the acute phase of myocardial infarct, successfully treated with surgery

The authors present a case of interventricular septal rupture with left ventricular free wall rupture post acute myocardial infarction operated on the third day after the onset of symptoms, by enfartectomy and application of a septal patch. Then, they compare this case with four cases referred in the literature, discussing the different and similar points between them. They emphasize the good results of this kind of surgery, but they also remark the need of an early diagnosis and surgery in these patients.     

Surgical treatment of postinfarction rupture of the interventricular septum

Between 1975 and 1990, 28 patients at our institution underwent surgical repair for rupture of the interventricular septum after acute myocardial infarction. Of the infarctions, 16 (57%) were in the inferior wall, and 12 (43%) were in the anterior wall. The most consistent clinical indication of septal rupture after acute infarction was a systolic murmur heard over the left sternal border. This finding was followed by hemodynamic deterioration in all patients. At the time of admission, 18 (64%) of the patients were in cardiogenic shock or multiple organ failure. Twenty-one patients (75%) underwent left heart catheterization; multivessel coronary artery disease was present in 4 (19%) of these patients. In 26 (93%) of the patients, the septum ruptured within the 1st 10 days after the infarction. Emergency surgery for septal rupture was performed using standard techniques in 25 (89%) of the patients. The transatrial transtricuspid approach for septal repair, although used in only 3 (11%) of our patients, provided a good surgical alternative to standard techniques and warrants further research. Excluding 1 late death, the overall operative mortality was 57% (16 patients); the hospital survival rate was 43% (12 patients). Cardiogenic shock was the most common predictor of a poor prognosis. Therefore, in order to avoid this complication, we recommend immediate surgical repair of postinfarction interventricular septal rupture.     

Serial changes in regional right ventricular free wall and left ventricular septal wall lengths during the first 4 to 5 years after index anterior wall myocardial infarction

Objectives. This study investigated serial changes in regional right ventricular free wall and interventricular septal wall lengths during the first 4 to 5 years after an index anterior wall myocardial infarction.Background. We previously demonstrated that remodeling after anterior wall myocardial infarction was a biventricular process; however, regional changes in biventricular topology were not investigated.Methods. Serial electron beam computed tomographic scanning was performed in 19 patients at five times (hospital discharge and at 6 weeks, 6 months, 1 year and 4 to 5 years) after an index anterior wall myocardial infarction, and global and regional right ventricular free wall and interventricular septal wall lengths were quantified.Results. At a mean (±SD) of 1,642 ± 171 days (4 to 5 years) after infarction, global end-diastolic and end-systolic right ventricular free wall and interventricular septal wall lengths increased in parallel by 13% to 23% as global left and right ventricular volumes increased 22% to 29% from hospital discharge to 4 to 5 years after infarction. When global right ventricular free wall was compared with interventricular septal wall lengths, percent increases at end-diastole and end-systole were not statistically different at any time during the study period. Distinct regional changes in both right ventricular free wall and interventricular septal wall lengths after infarction were most dramatic during the first 6 weeks and primarily confined to the most apical levels. However, further and significant increases in both were observed by 4 to 5 years after infarction.Conclusions. Changes in both right ventricular free wall and interventricular septal wall lengths were apparent during the 4 to 5 years after the index anterior wall infarction, and the combination of both contributed to global increases in right and left ventricular chamber volumes. Regional changes in both right ventricular free wall and interventricular septal wall lengths were almost exclusively confined to their respective apices and progressed generally in parallel; however, the cause-and-effect relation remains speculative at the present time.     

Clinical and anatomical features of acute myocardial infarction associated with double rupture of the interventricular septum and ventricular free wall]

Four patients with acute myocardial infarction (MI) complicating double rupture; interventricular septum and ventricular free wall ruptures, were studied. All patients had histories of hypertension, and pre-infarction angina pectoris of short duration less than 8 days without previous MI. The sites of infarction were anteroseptal in 2 patients and inferoposterior in the other 2. Only one case was complicated with mild pump failure (Killip class II). Blood pressure was adequately controlled after the onset of MI in all patients. Interventricular septal rupture occurred between 2 and 10 days after the onset of MI. Free wall rupture occurred between 2 and 22 days after MI. Types of free wall ruptures were oozing in 2 patients and blow-out in the other 2. Surgical repair was performed in 2 patients with the oozing type rupture, who however died soon after surgery. The autopsy findings were as follows: 3 patients had left ventricular free wall ruptures and one had right ventricular free wall rupture. One of the patients with left ventricular free wall rupture showed a secondary rupture of a pseudo-ventricular aneurysm. Postmortem coronary angiograms revealed 3 patients with single-vessel disease and one patient with double-vessel disease, indicating that coronary arterial lesions and complicated heart failure were not severe in these 4 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Case report: An unusual complication of clopidogrel

In an era of early and invasive therapeutic approaches, myocardial rupture has become an uncommon complication of myocardial infarction. While septal wall rupture most often leads to devastating haemodynamic consequences, free wall rupture is usually fatal. We report a case of a 48-year-old man in whom an incomplete myocardial rupture located in the inferior part of the interventricular septum was promptly detected during the acute phase of an inferior myocardial infarction treated by early percutaneous coronary angioplasty. A conservative rather than a surgical approach was decided with a favourable short-term outcome.     

Myocardial rupture after acute myocardial infarction. Ten year review.

Forty-nine patients with myocardial rupture complicating acute myocardial infarction were managed in our coronary care unit from 1972 to 1981: 33 patients with post-infarction ventricular septal defect, 12 patients with isolated rupture of the free wall of the left ventricle, and four patients with papillary muscle rupture. Nine of 19 patients (47%) who underwent surgical repair of a post-infarction ventricular septal defect survived. The major determinant of survival was the preoperative haemodynamic status. Ten of 13 patients (77%) who developed cardiogenic shock preoperatively died, while none of the six patients who were not in cardiogenic shock died. Survival was not related to the site or size of infarction, extent of coronary artery disease, or magnitude of the left to right shunt. There were no survivors among the 14 patients with post-infarction ventricular septal defect managed without surgical intervention. Seven of the 12 patients with isolated rupture of the free wall of the left ventricle developed mechanical cardiac arrest and died at the onset of rupture, but five patients developed subacute heart rupture and two of these patients survived after urgent surgical repair. Two of the four patients with papillary muscle rupture underwent mitral valve replacement, but both died in the early postoperative period; both patients who were not operated on died. Early detection and early surgical intervention are essential in the management of myocardial rupture complicating acute myocardial infarction.     

Effect of medical treatment of acute myocardial infarction in coronary care unit--study on its effect mainly on the cases with complication

Four hundred sixty-five patients with acute myocardial infarction who were treated in our coronary care unit in the past 14 years were classified into three stages (Stage I, II and III) for the purpose to study the effect of the treatment at CCU in each stage. The mortality in acute phase were 25.8%, 16.1% and 18.8% in Stages I, II and III, respectively. The mortality of cases admitted within 24 hours was 32.2% in Stage I, 27.1% in Stage II and 15.6% in Stage III, decreasing significantly (p less than 0.01) in Stage III. In cases of early hospitalization within 3 hours after the attack, the mortality in Stages I, II and III were 36.6%, 17.2% and 11.4%, decreasing in Stages II and III, specifically significant in Stage III compared with Stage I (p less than 0.01). The mortality in Class III of Killip's classification in each stage was 100% in Stage I, 33.3% in Stage II, and 16.7% in Stage III, and decreased significantly in Stages II and III (p less than 0.01). The mortality in Class IV are still high, although a decreasing tendency is observed as shown in figures such as 87.5% in Stage I, 62.5% in Stage II and 60% in Stage III. Thus, the mortality was markedly improved in cases which were hospitalized in early phase. Therefore, this result implies the importance of measures to promote early hospitalization including educational activity to appeal it. Early hospitalization in CCU is expected to minimize the death of acute myocardial infarction.     

Major causes of death from acute myocardial infarction in a coronary care unit

In order to define indications for newly developing aggressive managements for patients with acute myocardial infarction, an analysis of therapeutic results was made on 1,060 patients admitted to our coronary care unit (CCU). The total mortality was 14.9%, and 143 patients (13.5%) died from cardiac complications. These 143 patients were divided according to causes of death listed in Killip's classification. In the Killip class 4 group, mortality was as high as 86.6%, and all patients with previous infarction and/or hemodynamic abnormality of Forrester's subset 4 died. Pump failure caused death in 100 patients, of whom 69 were in a state of cardiogenic shock at the time of their admission. On the other hand, 58 patients, accounting for 40.6% of the cardiac deaths, were in Killip's class 1 or 2 at admission. In these 58 patients, 23 died from free wall rupture and/or perforation of the interventricular septum. Another 27 patients expired from reinfarction or infarct size extension and/or post-infarction angina. Thus, we can say that the major causes of death of patients in CCU are cardiogenic shock, reinfarction and cardiac rupture. We could not save these patients by using conventional CCU managements. Newly developing aggressive techniques, such as intracoronary thrombolysis and artificial hearts, seem to be indicated for these potentially fatal patients, while the effectiveness of these techniques should be verified as to such patients.     

Chronic effects of myocardial infarction on right ventricular function: a noninvasive assessment

To assess the chronic effects of myocardial infarction on right ventricular function, 48 subjects were studied utilizing radionuclide angiography and two-dimensional echocardiography. Ten were normal subjects (group I), 11 had previous inferior wall myocardial infarction (group II), 10 had previous anteroseptal infarction (group III), 11 had combined anteroseptal and inferior infarction (group IV) and 6 had extensive anterolateral infarction (group V). The mean (+/- standard deviation) left ventricular ejection fraction was 0.66 +/- 0.03 in group I, 0.58 +/- 0.02 in group II, 0.52 +/- 0.02 in group III, 0.33 +/- 0.03 in group IV and 0.33 +/- 0.01 in group V. No systematic correlation between left and right ventricular ejection fraction was observed among the groups. The mean right ventricular ejection fraction was significantly reduced in the presence of inferior myocardial infarction (0.30 +/- 0.03 in group II and 0.29 +/- 0.03 in group IV compared with 0.43 +/- 0.02 in group I [p less than 0.001]). The group II and IV patients also had increased (p less than 0.001) right ventricular end-diastolic area and decreased (p less than 0.001) right ventricular free wall motion by two-dimensional echocardiography. In the presence of anteroseptal infarction (group III), right ventricular free wall motion was increased (p less than 0.05) compared with normal subjects (group I). Thus, the effects of prior myocardial infarction on right ventricular function depend more on the location of infarction than on the extent of left ventricular dysfunction. Inferior infarction was commonly associated with reduced right ventricular ejection fraction and increased right ventricular end-diastolic area. The right ventricular free wall excursion was increased in the presence of anteroseptal infarction, suggested loss of contribution of interventricular septal contraction to right ventricular ejection.     

An echocardiographic study of interventricular septal motion in the Wolff-Parkinson-White syndrome.

Echocardiographic studies of interventricular septal motion were performed in 26 consecutive patients with the Wolff-Parkinson-White (WPW) syndrome and in ten normal subjects. All patients with types A or B pre-excitation were subclassified into groups I to IV on the basis of their electrocardiogram utilizing the method of Boineau and associates. In all 14 patients with type A (Group III or IV) pre-excitation, the motion of the interventricular septum and posterior left ventricular wall motion were normal. However, in 11 patients with type B (Group I) WPW an abnormal septal movement was noted. This was characterized in ten patients by an early systolic posterior motion, a subsequent anterior movement in mid systole, and the usual posterior septal motion beginning in late systole. In eight patients, including the one without early systolic posterior movement of the septum, the late systolic posterior movement was interrupted by a prominent septal notch. On e patient with type B (Group II) WPW was studied and exhibited normal septal and posterior wall motion. In one patient with a spontaneous change in the QRS complex from normal to a type B (Group I) WPW pattern, the septal motion was initially normal and abruptly changed following the first WPW beat. The onset of abnormal interventricular septal motion with type B pre-excitation QRS complexes strongly suggests that abnormal septal movement may be related to an altered sequence of ventricular depolarization during right ventricular pre-excitation.     

Post-infarction rupture of the interventricular septum. A report on 2 cases studied by color-coded Doppler

Rupture of interventricular septum is an infrequent but serious complication of acute myocardial infarction. We report the cases of two patients admitted to our department for acute myocardial infarction whose clinical course was complicated by rupture of the interventricular septum. They died from cardiogenic shock on the 13th and 6th days. Two dimensional and color coded echocardiography correctly detected the presence and the site of the rupture.     

Direct visualization of left ventricular free wall rupture by levocardiography.

Two cases of left ventricular free wall rupture and one case of combined left ventricular free wall and ventricular septal rupture are described where ventriculography played a key role in diagnosis. In all three cases of patients with acute myocardial infarction, identification and localization of the defect was made by angiography. This report illustrates the safety and feasibility of ventriculography in patients with suspected cardiac rupture.     

Rupture of the free wall of the left ventricle as the first manifestation of a myocardial infarct. A clinical case operated on with success]

A case of an undetected myocardial infarction in a patient with diabetes mellitus in which the first clinical sign was a syncope due to rupture of the left ventricular inferior wall is described. Survival was enhanced by a fast diagnosis (aided by the availability of an ECO 2D in the emergency room), by emergency pericardiocentesis with temporary haemodynamic stabilization and by prompt access to the Cardiosurgical Unit. A prompt diagnosis and treatment can allow the survival of patients, even in the extreme case that the ventricular wall rupture represents the first clinical manifestation of the myocardial infarction. The left ventricular free wall rupture in the course of myocardial infarction has a subacute pattern in about 30%, due to various mechanisms such as thrombosis or pericardial adherence over the ruptured wall.     

Natural history and prognosis of ischemic heart disease

Forty-four cases with myocardial rupture (33 with free wall rupture, 9 with interventricular septal perforation and 2 with papillary muscle rupture), all of which were ascertained by autopsy and/or at surgery, were analyzed. When the following 7 risk factors were actively managed in the acute stage of myocardial infarction, the incidence of myocardial rupture was significantly reduced: a) high blood pressure on admission, b) physical and emotional instability, c) recurrent chest pain, d) aged females, e) no history of angina or myocardial infarction, f) large myocardial infarction on ECG and g) the first 10 days after the attack of myocardial infarction. If cardiogenic shock occurs, surgery should be performed as soon as possible; if not, it should be delayed 3 weeks. The natural history of ischemic heart disease was analyzed in 400 medically-treated patients with significant coronary artery disease. They had been followed up continuously and periodically for more than one year. The prognosis of the patients with 3-vessel disease or left main trunk disease, those with poor left ventricular function (EF less than 30%) and of old age (greater than or equal to 60) and those who had a history of ischemic heart disease was poor. Follow-up study was done in 30 patients with variant angina. They often had life-threatening arrhythmias during attacks (8 ventricular tachycardia or ventricular fibrillation, 8 serious bradyarrhythmia). All patients with variant angina should be treated medically at first, and only patients with organic coronary artery disease and chest pain on effort in spite of the medical treatment should be considered as candidates for AC bypass surgery.     

Gunshot wounds: causing myocardial infarction, delayed ventricular septal defect, and congestive heart failure

Penetrating chest trauma can cause a wide variety of cardiac injuries, including myocardial contusion, damage to the interventricular septum, laceration of the coronary arteries, and free-wall rupture. Herein, we describe the case of a 21-year-old man who presented with congestive heart failure, which was secondary to an old myocardial infarction and complicated by the delayed formation of a ventricular septal defect. All of these conditions were attributable to multiple gunshot wounds that the patient had sustained 6 months earlier. Left ventricular angiography showed an apical aneurysm; a large, muscular, ventricular septal defect; and 19 gunshot pellets in the chest wall. Three months after aneurysmectomy and surgical closure of the septal defect, the patient had recovered fully and was asymptomatic.This case reaffirms the fact that substantial cardiac injuries can appear months after chest trauma. The possibility of traumatic ventricular septal defect should be considered in all multiple-trauma patients who develop a new heart murmur, even when overt chest-wall injury is absent.     

Complex ventricular septal rupture with dissection of the right ventricular wall in ischemic context

A 72-year-old man was admitted to the local hospital with non-ST elevation myocardial infarction. In the first 24 hours, a new onset apical murmur was heard. Transthoracic and transesophageal echocardiography showed interventricular septal (IVS) rupture and dissection of the right ventricle (RV) wall forming an echolucent pseudocavity that partially occupied the RV and communicated with the true RV cavity. Multislice computed tomography characterized in detail the IVS and RV wall dissection, and further showed the right coronary artery in the outer border of the RV and pseudocavity, excluding pericardial fluid. Despite surgical correction, progression to cardiogenic shock and death occurred 33 days after admission.     

Heart rupture as a complication of myocardial infarct in the acute stage. Case contributions and clinical course of survivors

Heart rupture was found in 25 (4.4%) of 560 patients with myocardial infarction admitted to the Coronary Care Unit of the Department of Cardiology, Padua Medical School. Ten (40%) of them had a breaking of the free wall, 10 the interventricular septum, 4 (16%) a papillary muscle and 1 (4%) the ventricular wall with formation of a pseudoaneurysm. Thirteen patients died suddenly, the other 12 (48%) had cardiac catheterisation and later surgery. Four patients with interventricular defect died immediately after surgery, the other patients were discharged. Mortality was 68%; 30% on the patients with VSD as well as those with papillary muscle rupture and pseudo aneurysm survived.