Ventricular free wall rupture following acute myocardial infarction

SUMMARY: Ventricular free wall rupture remains a dreaded complication of acute myocardial infarction. A dramatic fatal presentation is not universal and if recognized early, especially in its sub-acute form, a therapeutic intervention may be lifesaving. Changing trends in its natural history and the previously described pathological subtypes have emerged since the advent of thrombolysis. Although frequently unpredictable, certain clinical, echocardiographic and electrocardiographic signs should suggest the diagnosis. Moreover, knowledge of predisposing risk factors and a high index of suspicion are helpful in early recognition of this complication. In recent years, several different therapeutic approaches have been described including percutaneous seals and surgical mechanical closure of ventricular free wall rupture. In this review, we sought to highlight established and debatable aspects of this pathology to hopefully enhance prompt diagnosis and treatment by all clinicians caring for patients suffering acute myocardial infarction.     

Early diagnosis of subacute free wall rupture complicating acute myocardial infarction

Of 2608 consecutive patients with acute myocardial infarction,24 developed subacute free wall rupture (=0.92%; 95% C.I.=0.6–1.4).Clinical manifestations varied widely (shock on admission: 25%of cases; severe arrhythmias followed by shock: 17%; shock duringhospital stay: 42%; symptoms suggestive of infarct extensionwithout shock: 17%). The electrocardiograms were confusing ratherthan revealing: 56% of patients showed new ST segment elevationsof 0.2 to 1 mV in the infarct-related leads, while autopsy orcreatinine phosphokinase evidence of infarct extension was missing.In the first 21 cases, therefore, no definitive diagnosis wasmade before autopsy. Using 197 infarct patients in cardiogenic shock or with infarctextension during the acute stage, i.e. a patient group withcomparable clinical manifestations, as control group, a logisticregression model was generated in which the variables age, lateralwall involvement and history of hypertension were used for estimatingthe probability of subacute rupture. In fact, probability mayrise to more than 40% in major subgroups. As death occurred after a median interval of 8 h (45 min–6.5weeks) following the onset of rupture symptoms, echo-cardiographymust be performed urgently in all cases presenting symptomsof shock or infarct extension. Pretest probability which canbe roughly estimated from our model as well as sensitivity andspecifity of individual echocardiographic or clinical parametersare indispensable for correct therapeutic decisions. The routineapplication of this algorithm in our department contributedto a timely diagnosis in the last three consecutive cases ofwhom one patient survived.     

Ventricular free wall rupture following acute myocardial infarction: a two-dimensional echocardiographic assessment

To assess the usefulness of two-dimensional echocardiography (2DE) in diagnosing ventricular free wall rupture following acute myocardial infarction, we studied the 2DE findings and the clinical pictures of seven consecutive patients with ventricular free wall rupture confirmed at the time of surgery or autopsy. Three patients had acute rupture; four, subacute rupture. All patients apparently had circulatory collapse despite continuing electrical activity at the onset of cardiac rupture. Four patients with subacute rupture recovered. In all patients, mild pericardial effusion was imaged by 2DE; however, this was not characteristic for cardiac rupture. In the patients with acute rupture, active left ventricular contractions were not observed after each QRS complex of the electrocardiogram. However, weak mitral valve motion was recorded at the time of cardiopulmonary resuscitation. The interesting and constant finding in acute rupture was the right ventricular collapse observed throughout the cardiac cycle. Diastolic right ventricular collapse was consistently observed in patients with subacute rupture, immediately after recovery from cardiogenic shock. Subacute cardiac rupture is a potentially curable lesion, and the clinical features and quick 2DE confirmation of cardiac tamponade allowed immediate surgery which saved two of the four patients.     

Ventricular free wall and septal rupture (double rupture): A “pseudocomplication” during post-infarction laser angioplasty

We report the rare occurrence of double rupture of the myocardium occurring immediately following successful laser recanalization of an occluded right coronary artery in a 72-year-old woman 5 days following infero-posterior myocardial infarction. © 1993 Wiiey-Liss, Inc.     

Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size

Left ventricular rupture was studied in 849 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size. Although documented rupture occurred in only 14 cases (1.7%), it accounted for 14% of in-hospital mortality. Seven of the 14 ruptures occurred within 2 days and 10 within 4 days of the MB-creatine kinase-determined onset of infarction. Three easily determined baseline characteristics defined a set of patients with a markedly increased risk of myocardial rupture. Rupture was 9.2 times more likely to occur in patients with all of the following characteristics than in the remaining patients: (1) no history of previous angina or myocardial infarction, (2) ST segment elevation or signs of Q wave development on the initial ECG, and (3) peak MB-creatine kinase value (greater than or equal to 150 IU/L). The risk of myocardial rupture with these three characteristics was 5.5%. Although these predictors are likely to be of little therapeutic value for free wall rupture, since most patients with that complication die within minutes of its onset, they may aid in alerting physicians to the early diagnosis and timely surgical correction of ventricular septal rupture.     

Ventricular septal rupture complicating surgically treated left ventricular free wall rupture in a patient with acute myocardial infarction. A case report

There is a group of rare but serious complications of acute myocardial infarction (AMI), including free wall rupture (FWR) and, less frequent, ventricular septal rupture (VSR). Urgent surgery combined with simultaneous CABG is usually a treatment of choice. We present a case of a 65-year-old male with AMI, who developed cardiogenic shock due to cardiac tamponade as a result of FWR. The patient was successfully resuscitated and operated. During postoperative treatment parasternal systolic murmur was audible and VSR diagnosis was confirmed. Three months after AMI the AMPLAZER Muscular VSD Occluder was successfully implanted. The follow-up period was uneventful.     

A subacute left ventricular free wall rupture after thrombolytic and glycoprotein IIb/IIIa inhibitor treatment: an overlooked finding of left ventriculography

Subacute left ventricular free wall rupture is a rare complication in acute myocardial infarction. With the increasing use of thrombolytic agents and glycoprotein IIb/IIIa inhibitors, this complication has been increasing recently. We report a case of subacute cardiac rupture with frank pericardial effusion receiving thrombolytic and glycoprotein IIb/IIIa inhibitor therapies.     

Postinfarction left ventricular free wall rupture repaired successfully

Left ventricular free wall rupture is a well-recognized complication of myocardial infarction and a frequent cause of death. A 49-year-old man was successfully treated for a left ventricular free wall rupture that occurred on the third day after an anterior myocardial infarction. Concomitant myocardial revascularization was performed.     

Successful management of left ventricular free wall rupture

Cardiac rupture is a complication of myocardial infarction with an exceedingly high mortality rate. Imaging modalities, such as echocardiography, have facilitated premortem diagnosis, thus increasing chances of survival. A review of pertinent literature is accompanied by a case report that details an episode of left ventricular free wall rupture and its successful outcome.     

Left ventricular free wall rupture after acute myocardial infarction(The 21th case)

患女性，69岁，退休，以胸闷16h入院。患活动后发病，逐渐出现呼吸困难。否认既往冠心病病史，合并高血压。入院时查体体温36．5℃，心率110次／min，呼吸27次／min，血压90／60mmHg。精神差，心律齐，心音低钝，各瓣膜区未闻及杂音。心尖部可闻及舒张期奔马律，双肺可闻及中到大量湿哕音。急诊心电图：窦性心动过速，前壁及高侧壁导联ST段抬高0．1～0．3mV，Q波形成。心肌酶升高。诊断急性广泛前壁心肌梗死。[第一段]     

An unusual presentation of left ventricular free wall rupture

Left ventricular free wall rupture (LVFWR) is one of the most lethal complications following myocardial infarction. It accounts for approximately 12% to 21% of all in-hospital deaths following myocardial infarction. The majority of patients die shortly after LVFWR from instantaneous pericardial tamponade and hemodynamic collapse. However, up to one-third of cases are subacute in nature, allowing limited time for emergent surgical repair to prevent sudden death. A high index of suspicion and timely use of diagnostic tests are important in recognizing cases. The present report describes the case of a 69-year-old man who initially presented with acute pericardial tamponade and was subsequently diagnosed with LVFWR in the operating room as the cause of his hemopericardium. The pathology, diagnosis and management of LVFWR are reviewed.     

Left ventricular free wall rupture during dobutamine stress echocardiography

Dobutamine stress echocardiography is associated with a very low rate of serious complications, lower than 0.5% (death, infarction or sustained ventricular tachycardia). We report the case of a 75 year-old female patient that suffered a fatal left ventricular free wall rupture during a dobutamine stress echocardiography after acute myocardial infarction.     

Myocardial free wall rupture and thrombolytic therapy in acute myocardial infarction

We investigated the relation between myocardial free wall rupture and thrombolytic therapy in 200 patients with acute myocardial infarction (AMI). Ten of 200 patients (5.0%) were complicated with cardiac rupture, and all of them died within 70 hours after the onset (29% of the deceased after AMI). The pathophysiologic study of 5 patients undergoing autopsy after cardiac rupture was performed. In 4 patients receiving thrombolysis, autopsy revealed massive hemorrhagic infarction and teared lesion near the center of infarcted area. We assessed that the location of teared lesion might be influenced by broad hemorrhagic infarcted area following thrombolytic therapy. The incidence of cardiac rupture was slightly higher in the group receiving thrombolysis in the early stage of AMI than conventional treatment group. Among the patients receiving thrombolytic therapy, some cases revealed markedly increased fibrinolytic activity. This suggested that such elevated fibrinolytic activity might induce massive hemorrhagic infarction and might be an important factor contributing to the cardiac rupture. Thrombolytic therapy has been frequently reported to improve cardiac function and prognosis, but our study suggests that thrombolytic therapy must be evaluated moreover as one of the risk factors of cardiac rupture.     

Delayed two-step free wall rupture of the right and left ventricular wall after myocardial infarction

We present a 68-year-old female who suffered extensive complications after severe myocardial infarction (MI) in the circumflex (CX) territory. At 24 hours after the initial event, the patient presented with a covered right ventricular free wall rupture (FWR) which was followed by a rupture of the left posterior wall ten days later. We report here on a rare case of delayed two-step biventricular FWR after severe MI in the CX territory.     

Subacute left ventricular free wall rupture following acute myocardial infarction: Bedside hemodynamics,differential diagnosis,and treatment

Six patients with subacute left ventricular free wall rupture (anatomically proved) following acute myocardial infarction are presented. Diagnosis of cardiac rupture in every case was suspected several hours before death or surgical intervention, when clinical and hemodynamic data of cardiac tamponade were found. In three patients right atrial pressure decreased with inspiration and in the other three cases it did not show any modification. These latter three patients had associated right ventricular infarction; the abnormal respiratory behavior could be explained by restriction produced by a noncompliant right ventricle. All six patients improved initially with medical treatment (inotropics and fluid infusion) and three of them were operated upon. One of the latter patients died on the eighteenth postoperative day of extracardiac causes and two are long-term survivors.     

Myocardial laser coagulation for free wall rupture following acute infarction

A 73-year-old woman was diagnosed with ventricular free wall rupture following acute myocardial infarction. The lesion was repaired with laser coagulation, fibrinogen-thrombin glue application, and patch reinforcement. Five years after surgery, the patient was in New York Heart Association class I.