Acute mechanical complications in patients suffering from acute myocardial infarction

Introduction

Mechanical complications of myocardial infarction are direct consequences of anatomic and pathological changes occurring in ischemic cardiac tissue. After a coronary occlusion, there is a lack in blood perfusion and in oxygen supply that cause functional, morphological and biochemical changes. Within the first 30 min from the occlusion, reversible changes happen: macroscopic and microscopic changes are not occurring yet, but myofibrils start to relax, and cells start to suffer. After 30 min, ischemic necrosis begins, and the irreversible damage occurs. After 2-4 h, complete necrosis of myocardial cells may occur, depending on the coronary collateral circulation, the severity and the time of coronary vessel occlusion and the individual demand for oxygen and nutrients. Loss of myocardial vitality is complete after 6-12 h from the onset of coronary occlusion. Within one week, macrophagic phagocytosis and irreversible collagen damage begin, and tissue becomes less resistant; in that period, myocardial tissue becomes more vulnerable and weaker and heart ruptures are more frequent^[1,2].

For the purpose of this review we analysed one of the 5 categories of complications of acute myocardial infarction (AMI) named as mechanical complications after AMI, such as ventricular free wall rupture, ventricular septal defect, papillary muscle rupture of mitral valve. The other 4 categories (electrical complication, inflammatory, ischemic and embolic complication) were exclude from this article.

Most of all mechanical complications of myocardial infarction require an urgent/emergent surgical therapy. Meanwhile, initial diagnosis should be rapid and initial medical therapy should be promptly started, to improve coronary perfusion, stabilise the haemodynamic condition and ameliorate the peripheral perfusion. Supplement oxygen, mechanical ventilatory support whether necessary, analgesic therapy, crystalloid infusion and inotropic agents represent usually the first medical approach. In very critical and challenging poor clinical and hemodynamic status, requirement of an intra-aortic balloon pump (IABP) or even a more advanced temporary circulatory support such as veno-arterial extracorporeal membrane oxygenation are valid option to manage and stabilise the patient^[3].

Left ventricular free wall rupture

Left ventricular free wall rupture (LVFWR) is account for 15% after AMI and it is more frequent than septal or papillary muscle rupture^[4,5]. LVFWR may occur at any time after myocardial infarction, usually within the first 3-5 days but may happen up two 15 days^[6]. However, at least 25% of heart rupture occurs within the first 24 h. The short-term mortality remains very high even rapid diagnosis and surgery. Data from one of the largest multicentre trial, the Global Registry of Acute Coronary Events study, report an incidence of LVFWR of 0.2% with an in-hospital mortality of 80%^[7]. In more recent retrospective studies and reviews, the early mortality was ranging between 14% to 35%, according the initial haemodynamic status, the type of LVFWR and the type of surgical repair^[3,8-10].

Three types of cardiac rupture of cardiac rupture were classified as follows: acute, subacute, and chronic^[11]. The acute rupture (also named “blow-out” rupture) is characterized by a massive haemopericardium [Figure 1] and most of patients presented with electro-mechanical dissociation and sudden cardiac death. When the rupture area is smaller, the bleeding is stopped by clot formation or pericardial adhesions. This type is called also “oozing” rupture, and patients presented with hypotension and arrhythmias and clinical signs of pericardial tamponade.

Figure 1. Massive hemopericardium following “blow-out” left ventricular free wall rupture

The accuracy of diagnosis of subacute LVFWR requires a high degree of suspicion^[12]. Trans-thoracic echocardiogram is the first diagnostic tool as most of patients show pericardial effusion in addition to echogenic images, in an early period after AMI. Due to these findings, echocardiogram has a high level of sensitivity and specificity (more than 95%) for the LVFWR diagnosis^[13]. Furthermore, when pericardial effusion is more than 10 mm in patients with a recent diagnosis of AMI with ST elevation, the probability of 30-day mortality is as high as 43%^[14]. When pericardial effusion is associated with hypotension and bradycardia, rapid pericardiocentesis is useful to stabilize the patients before taking the patients for emergency surgical therapy.

Surgical repair of the rupture site is the gold and definitive treatment. Surgery may be performed in different ways and different techniques according to the hemodynamic status and the types of cardiac rupture. In a recent review, Matteucci et al.^[10] described the following surgical techniques: (1) linear closure [Figure 2] or infartectomy associated to closure of the defect with a prosthetic patch when the LVFWR is a blow-out type^[3]; (2) covering patch technique or sutureless technique (named also “patch and glue”) in case of oozing LVFWR [Figure 3]^[3,8]. Operations can be performed with or without cardiopulmonary bypass. Off-pump procedure is the technique of choice in case of oozing LVFWR and patients in stable conditions. Some authors heave recently reported newer surgical strategies, usually performed in presence of oozing by using different materials such as ready-to-use haemostatic collagen sponges^[3,8,15] and newer acellular xenogeneic extracellular matrix patches [Figure 4]^[16].

Figure 2. Linear closure of a “blow-out” left ventricular free wall rupture (inferior wall)

Figure 3. Sutureless techinique with autologous pericardial patch in “oozing” left ventricual free wall rupture

Figure 4. Oozing anterior left ventricular free wall rupture (A); ready-to-use haemostatic collagen sponges (B)

Preoperative and postoperative insertion of IABP is advocated by some authors even when patients presented in stable haemodynamic status, with the aim to reduce the oxygen demand, the left ventricle wall tension and the left ventricle afterload^[17,18]. This approach may reduce the risk of re-rupture during the early postoperative period. In the last 20 years, ECMO has emerged as a rescue tool to warrant a rapid haemodynamic stability in such patients presented with acute cardiogenic shock or even cardiac arrest^[19,20]. ECMO may be use also to stabilize patients affected by LVFWR in referring hospitals^[21,22]. However, there is a lack of evidence of any benefit of preoperative and perioperative ECMO in patients affected from LVFWR due to the very low numbers of reports regarding this specific topic.

In-hospital mortality is extremely variable, ranging from 12% to 61% among different Institutions^[3,8,23-25]. Despite the relative high in-hospital mortality, midterm and long term survival show encouraging outcome [Table 1].

Ventricular septal defect

The incidence of VSD has been estimated between 1% and 2% of all patients suffering from acute myocardial infarctions even if the advent of reperfusion therapy has decreased this value below 0.5%. Despite the low incidence, the early mortality is still high, reaching about 60%-70%. Without surgical treatment, only about 10% of patients survives after 3 months^[26].

Risk factors for VSD include advanced age, hypertension, absence of angina, extensive myocardial infarction and single vessel disease^[27,28].

The acute rupture occurs 3-7 days after a wide transmural infarction but may occur rarely after 2 weeks^[28,29]. VSD results in a left-to-right shunt which is the main cause of low cardiac output, decreased urine output, shortness of breath, altered mental status and finally cardiogenic shock^[30]. At physical examination, a harsh and loud pan-systolic murmur at the left lower sternal border is present in over 90% of cases. A palpable thrill can be detected in up to 50% of patients.

VSDs has been categorized in two other categories: simple and complex. Simple rupture is a discrete lesion, with defect located at a similar level in both ventricles. That is typical pattern of anterior myocardial infarction. Inferior myocardial infarction usually is associate to a complex type^[31,32].

In both cases, the defect may vary in size from some mm to more than 15 mm. The size of defect may affect the magnitude of left-to-right shunting, and therefore influencing the clinical presentation and the likelihood of survival. Trans-thoracic and transesophageal echocardiography with Doppler imaging is considered a high sensitive and specific diagnostic tool for immediate diagnosis.

Medical therapy is usually managed with the use of vasodilators, which reduce afterload and decrease left ventricular pressure and the left to right shunt, with inotropic agents, which may increase the cardiac output, diuretics, and IABP. Use of preoperative ECMO was reported in patients with refractory cardiogenic shock^[33,34]. Some authors have reported the use of the Impella to achieve haemodynamic stabilization with acceptable results. However, the use of Impella is limited in selected patients and only few experiences with few patients were published so far^[35-37].

Timing of surgery is still debating. Recently, Papalexopoulou and co-workers published a review reporting that early surgery is advocated if VSD size is more than 15 mm and an instable haemodynamic. While delayed surgery might be performed up to 3 or 4 weeks in case of clear hemodynamic clinical status. Emergency surgery should be performed in patients with refractory cardiogenic shock and rapid deterioration^[38]. A review form the Society of Thoracic Surgeon National Database identifies that mortality of patients who underwent surgery within 7 days was approaching to 54% compared to patients who underwent surgery after 7 days. In this latter clinical scenario, mortality was 18%^[39]. Early mortality is affected also from the VSD location. In patients with basal or inferior VSD mortality is as high as 70%^[34]. Apical or anterior VSD are affected from a lower early mortality (30%)^[27].

Right ventricular dysfunction is an issue to be considered in VSD. The right ventricular dysfunction maybe consequence of right ventricular infarction and right ventricle acute overload depending on the magnificence of the left-to-right shunt.

Multiple surgical techniques have been described [Figure 5]. Apical amputation is the simpler in patients with apical defects. Other techniques involve infarct exclusion and defect closure with a patch (biological or synthetic) using both stitches or glues^[40,41]. Despite continuous advances in surgical approaches, operative mortality remains high (ranging from 20% to 71.4%), with no clear differences between different techniques^[41-43]. Female gender and depressed left ventricular dysfunction at admission are linked with a high hospital death^[43].

Figure 5. Apical ventricular septal defect (A); prosthetic patch for septal defect closure (B)

Table 2 reports the in-hospital mortality rates and long-term survival percentages of studies with relatively large number of patients.

Percutaneous closure of the VSD remains an attractive alternative to surgical repair mainly in extremely high-risks patients with reasonable results. Despite the in-hospital mortality is graved from a relatively high incidence (from 20% up to 46%), the patients who survived to discharged had a very acceptable long-term survival^[43,49].

Papillary muscle rupture of mitral valve

Papillary muscle rupture (PMR) is a rare entity and occurs in less than 0.5% of patients with acute myocardial infarction^[50]. Timing of rupture is ranging between 2 and 7 days, but 80% occurs in 7 days.

Mortality may be as high as 50% in the first 24 h, and rises up to 90% within the first week^[51].

Anterior papillary muscles receive a dual blood coronary supply, while posterior papillary muscle receives blood from the only right coronary artery. Due to this anatomical difference, PMR is most common after an inferior acute myocardial infarction, because the posteromedial papillary muscle is most often involved.

Doppler transthoracic and transesophageal echocardiography is the gold diagnostic tool. Transesophageal echocardiography has a very high diagnostic accuracy approaching to 100%^[52] for the evidence of a tear in papillary tissue and the flail of mitral valve leaflet leading to severe mitral regurgitation [Figure 6].

Figure 6. Transesophageal echocardiographic evidence of papillary muscle rupture

Emergent or urgent surgery is the only therapy for PMR, despite operative mortality rises up to 20%-39%^[53-55]. Medical therapy before surgery aims to reach a hemodynamic stability and includes aggressive afterload reduction to decrease the huge regurgitant fraction by using nitrates, sodium nitroprusside, diuretics, IABP. The use of ECMO was also reported.

Surgical technique depends upon the location and the type of rupture. In case of partial PMR, surgeons usually attempt for a repair of mitral valve. However, a surgical repair of the papillary muscle head is really rare. In case of complete PMR, mitral valve replacement becomes the treatment of choice Figure 7^[53,54].

Figure 7. Surgical view of papillary position (A); posterior mitral leaflet and portion of papillary muscle (B); bi-leaflet prosthetic mechanical valve in mitral position (C)

Long-term survival of patients who underwent mitral valve replacement for PMR is very acceptable, with a 5-year survival rate ranging between 60%-70%^[56,57].

Table 3 reports the in-hospital mortality rates and long-term survival percentages of studies with relatively large number of patients.

Conclusion

Mechanical complications after acute myocardial infarction are still affected by high 30-day mortality and poor long-term survival. The incidence of such complications is reduced in the post thrombolysis era, but the perioperative surgery continues to be relatively high. The diagnosis should be as prompt as possible, since in case of acute cardiogenic shock the surgery should be performed very early to increase the perioperative survival. Rescue tool as ECMO is an emerged therapy to stabile patients and even allowing the stabilization in referring hospital.