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Broken hearts.

A man is as old as his arteries (Thomas Sydenham)

In cardiology broken hearts are assimilated with myocardial ruptures which are often fatal complications of myocardial infarctions, more and more frequent at young ages, evolving with major complications. It is the vascular age that matters though, rather than the biological age. Myocardial rupture is a relatively common finding in patients dying of an acute myocardial infarction; its incidence ranges from 0.93 to 2.7% according to different statistics (Yip et al 2003), but appears to have decreased in patients undergoing primary percutaneous intervention for AMI. It causes death directly in 8% of patients (Reddy et al 1989). A rare but catastrophic form of this complication is the left ventricular free wall rupture (LVFWR), whose incidence is lowered when primary percutaneous intervention can be performed. (Amir et al 2005)

Nothing is less in our power than the heart (Jean Jacques Rousseau)

With a view to assessing the current incidence and risk factors for cardiac rupture, we studied the AMI patients admitted between January and December 2013 in Georgescu Institute of Cardiovascular Diseases, but only 17 patients had cardiac rupture. In general, all patients presented frequent comorbidities and a rather old age (between 56 and 85 years), with a median age of 73.1 years.

Classic LVFWR usually produces symptoms within the first 24 hours after an AMI and almost always by the end of the first week (Zaffoli et al 2012); its clinical manifestations depend on both the amount and the rate of intrapericardial bleeding. It varies from a catastrophic event, with an acute tear in the infracted myocardium leading to immediate death--acute rupture, or slow and incomplete tear leading to a late rupture, subacute rupture. (Vervaeke et al 2014)

An acute tear in the infracted myocardium characterizes the early rupture, with a preference for anterior sites. It occurs in up to 10% of the in-hospital deaths following AMI (usually between 3 to 6 days) (Reddy et al). LVFWR is then a devastating event and only a few patients may reach the operating room alive. In most cases, sudden hemodynamic collapse is followed quickly by electromechanical dissociation and death.

In some cases, a blood clot will seal pericardial leaks and form a left ventricular pseudoaneurysm. A subacute variant of LVFWR, marked by slow repetitive bleeding, occurs in approximately one third of cases and are less frequent in patients with successful reperfusion (Gosal et al 2008; Zoffoli et al 2012). Unlike patients with classic LVFWR, patients with the subacute variant may survive until emergency surgery can be performed. They are usually accompanied by a moderate to severe pericardial effusion without haemodynamic compromise.

Incomplete rupture may occur when the thrombus and haematoma together with the pericardium seal the rupture of the left ventricle and develop into a pseudo-aneurysm. (RoaCastro et al 2012)

If one of the traditional risk factors of LVFWR is delayed hospitalization, in our case the time interval to hospital presentation was as follows: 23.5 % were presented in the first 6 hours of the onset of chest pain (all of them were women), 41.1 % were presented between 6 and 12 hours and 35.2 % were presented in more than 12 hours. Chest pain was the most frequent symptom at presentation and it was reported on admission by all men, and only by 62.8% women. Myocardial rupture occurred at a median of 4.7 days of evolution, with a range between 1 and 18 days. In 92.8% of patients evaluated by echocardiography, the rupture was localized on the left ventricular free wall, only 7.2% being on the right ventricular free wall. Depending on their location, myocardial infactions had the following characteristics: 58.8 % were on the anterior wall, 29.4 % on the inferior and right ventricular wall, and 17% were on the inferior wall.

Other reported risk factors are (older) age, (female) sex, previous hypertension, and a first lateral or anterior wall AMI, ST-segment elevation or Qwave development on the initial ECG, peak MB-creatine kinase above 150 UI/L, delayed reperfusion, absence of left ventricular hypertrophy, heart failure, prolonged angina and delayed hospitalization (Gosal et al 2008). Contrary to several reports, steroid use and late thrombolysis do not appear to increase the risk of LVFWR (Amir et al 2005; Giugliano et al 2003). In our study there were no significant sex and comorbidity-related differences, compared with the classic risk profile of myocardial rupture. Most patients had a delayed presentation, with chest pain and anterior AML New onset sustained arrhythmias (atrial fibrillation, ventricular tachycardia and fibrillation) were presented in 64.6% of all AMI patients and they may represent another important risk factor for myocardial rupture in AMI patients.

The cardiac rupture may be clinically undetected and mostly identified on a routine post-infarction echocardiogram. Several studies have tried to identify the premonitory signs and symptoms of fatal LVFWR (Figueras et al 1997; Raitt et al 1993). Prodromal manifestations reported so far include persistent chest pain (often erroneously attributed to ischemia), intractable vomiting, restlessness, persistent ST segment elevation, and positive T-wave deflection that persists for 72 hours after the onset of chest pain (Amir et al 2005; Raitt et al 1993). Other classic signs of cardiac tamponade, including pulsus paradoxus and diastolic pressure equalization, are usually absent. Electromechanical dissociation may occur but has a limited diagnostic value. (Figueras et al 1997)

Echocardiography is considered to be the best choice for the definitive diagnosis of LVFWR. The main echocardiographic findings in patients with LVFWR are pericardial effusion and intrapericardial echoes; occasionally, we will find a right-heart collapse or the actual tear itself. Echocardiography has a diagnostic sensitivity of 100% and a specificity of 93% (Mittle et al 2003). Although hemopericardium may result from thrombolytic and glycoprotein Ilb/IIIa inhibitor therapy, LVFWR should always be considered the leading diagnosis in a patient with AMI who is hypotensive and has pericardial effusion. Nearly a quarter of our patients had a low ejection fraction with a median of 29.4% and 17.6% had a ventricular aneurysm. As the patients hospitalized with myocardial rupture were with multiple comorbiditics, the in-hospital mortality in our case was 100%.

Conventional coronary angiography was performed in all patients and revealed the two-vessel disease in more than half of the patients, only one patient having normal coronary arteries (the Tako-Tsubo syndrome).

The definitive treatment for LVFWR is emergency surgical repair; most often, pericardial patch placement is performed with either biological glue or epicardial sutures. Other surgical techniques include infarctectomy with patch placement and ventricular wall reconstruction (Attia et al 2010). Temporary therapeutic measures include rapid fluid infusion, administration of positive inotropic agents, and pericardiocentesis. Intra-aortic balloon pump (IABP) support is a widely accepted treatment for ventricular septal rupture complicating AMI (Bimbaum et al 2002). However, its role in patients with LVFWR is less clear (Fig. 1).

81 patients were prospectively analysed and assigned to different groups on the basis of their response to initial treatment (Figueras et al 1997). A self-selected group of 19 of 81 patients was managed conservatively with intravenous fluid, inotropic support, pericardiocentesis (n = 3) and strict bed rest. In-hospital mortality was 22% and mid-term survival was good at 77%. On the surgically treated arm, the article lacks data about short- and mid-term survival. Long-term survival was 13%. The surgical cohort of patients was critically unstable preoperatively.

In a prospective study a total of 29 patients with LVFWR were evaluated (Iemura et al 2001). Twelve patients died within 2 hours of haemodynamic crisis, before referral to a cardiac surgeon. The remaining 17 patients were treated with surgical repair, 12 with cardiopulmonary bypass support and 5 without it. Ruptures were labelled as "blow-out" in 3 and "oozing" in 14 patients. Surgical repair included infarctectomy and patch, patch repair, direct suture and sutureless technique with or without bypass. The overall survival rates for patients with blow-out type ruptures and those with subacute or oozing-type ruptures were 67 and 92%, respectively. The operative (30-day) mortality was 12%.

A cohort study of 32 consecutive patients was conducted between June 1993 and May 2006, with an average age of 73 (range 55-96) years (Sakaguchi et al 2008). The surgical technique in case was autologous patch-and-glue repair. Six patients had percutaneous cardiopulmonary support, but 26 were treated without cardiopulmonary bypass. Twenty patients required intra-aortic balloon pumps (IABP). Six patients had preoperative pericardiocentesis. The operative (30-day) mortality was 15.6% (n = 5). Of the 5 deaths, two had reruptures, two died of severe heart failure and one died of cerebral infarction. One patient developed LV pseudoaneurysm. The 5-year survival was 74%. We are thus told of the advantages of the sutureless treatment in the surgically treated group.

A case treated with intra-pericardial thrombin injections (Lee et al 2012) gave a favourable outcome for a patient who presented myocardial rupture and cardiac tamponade, following an acute myocardial infarction. We thus see the use and feasibility of an pericardial thrombin injection, acting as a haemostat and sealing agent for the treatment of post-infarction myocardial rupture.

A cohort study of patients with serious haemodynamic compromise secondary to LVFWR was conducted between October 2010 and May 2013 (Aoyagi et al 2014). Three patients underwent surgery by a sutureless repair technique: i.e. applying a sheet of fibrin adhesive collagen fleece (TachoComb), secured to the infarcted area by manual compression. Furthermore, several sheets of absorbable gelatin sponge (Gelfoam) were glued onto the collagen fleece in layers. Two patients survived. However, one patient died on Day 10 post-surgery, probably because of recurrent rupture, and another patient developed an LV aneurysm 4 months after repair. This sutureless technique points out the option of surgical treatment where unstable patients require urgent intervention without coronary perfusion pressure. Careful follow-up would be mandatory, considering the late complications.

Each heart is a world (John Caspar Lavater)

To conclude, surgery is superior to conservative management for patients presenting LVFWR post-AMI. Successful conservative strategy has little support in literature, apart from a few articles describing conservative treatment, which is only possible in a self-selected group of oozing or subacute-type rupture. Nevertheless, it may be an option in extremely high-risk groups (especially older patients). A surgical technique has evolved over the past 3 decades from infarctectomy and patch reconstruction to sutureless repair. The viable myocardium to determine the extent of myocardial resection in the presence of AMI, leading to significant morbidity and mortality postoperatively in patients treated with resection and suturing technique is difficult to assess. Repair involving cardiopulmonary bypass is disadvantaged by systemic heparinization and continuous oozing of blood through the necrotic areas of the myocardium adjacent to the primary site of infarction, which may lead to aneurysm formation. Distinct advantages of the sutureless technique are simplicity, speed, reproducibility, its being technically less challenging. There is an additional theoretical benefit of preserving LV geometry with patch-and-glue repair. However, the sutureless technique may not be suitable for patients with concomitant mechanical complication of AML (Nasir et al 2014)

Patients with myocardial rupture following acute myocardial infarction represent a management challenge to the clinician, which means that it is necessary to conduct more extensive studies in order to provide answers to whatever questions.

References

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Liviu Macovei Grigore T. Popa University of Medicine

Larisa Anghel Grigore T. Popa University of Medicine

Catalina Arsenescu Georgescu Grigore T. Popa University of Medicine

Correspondence concerning this article may be addressed to liviughmacovei@yahoo.com, larisa_med86@yahoo.com or catalina.arsenescu@gmail.com.
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Author:Macovei, Liviu; Anghel, Larisa; Georgescu, Catalina Arsenescu
Publication:Romanian Journal of Artistic Creativity
Date:Sep 22, 2014
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