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Hong Kong Journal of Emergency Medicine Ventricular free wall rupture after myocardial infarction F Lateef and N Nimbkar Patients with their first myocardial infarction (MI), who present to the emergency department many hours after the onset of chest pain, who appear to be improving but suddenly develop new chest pain and unexpected hypotension (with or without signs of cardiac tamponade), should be suspected of having ventricular free wall rupture (VFWR). The mainstay of treatment is surgery. These patients may be managed with the administration of fluids, cautious use of inotropes and echocardiographic scanning, which should be performed on an emergent basis, while being prepared to be moved to the emergency surgical suite. However, at no cost should surgery be delayed. This paper reviews the current literature of VFWR after MI, a condition which remains difficult to diagnose, in many aspects, to this day. The review examines the historical background, incidence, postulated risk factors, clinical presentation, investigations and management. (Hong Kong j.emerg.med. 2003;10:238-246) Keywords: Cardiac tamponade, cardiogenic shock, echocardiography, electrocardiography, post-infarction heart rupture "It seems that a person dies from a broken heart, not in young adult life from a great grief or emotion, but usually in old age, on account of diseased coronaries…" Krumbhaar and Crowell 1 Background Current awareness of the health care profession in treating arrhythmias after myocardial infarction (MI) and the effectiveness of their treatment have brought myocardial pump failure and cardiac rupture to prominence, as causes of early mortality. Myocardial pump failure is more common than cardiac rupture. Sh o r t o f m e c h a n i c a l d e v i c e s a n d / o r c a rd i a c transplantation the prognosis of post-infarct early Correspondence to: Fatimah Lateef, MBBS, FRCSEd Singapore General Hospital, Department of Emergency Medicine, Outram Road, Singapore 169608 Email: [email protected] Uniformed Services University of Health Sciences, Bethesda, Maryland, USA Narayan Nimbkar, MS, FRCSEd, FACS heart failure is not significantly improved by treatment. Rupture of cardiac muscle can manifest as perforation of the inter-ventricular septum, papillary muscle rupture or ventricular free wall rupture (VFWR), with the left being more common than the right. Early and successful treatment of left ventricular free wall rupture (LVFWR) has a distinct salutary effect on the overall prognosis of MI. William Harvey in 1647 described cardiac rupture as a finding at autopsy of a knight who suffered severe chest pain. 2 Morgagni, who had the misfortune of dying from this malady, had collected 10 cases by 1765.3 An English Surgeon Joseph Hodgron, in 1850, first suggested an association of coronary artery obstruction and cardiac rupture. 4 This was quickly followed by the landmark observations of Malmsten (1861), 5 Winsor (1880) 6 and Steven (1884). 7 Krumbhaar and Crowell et al1 in 1925 cited 564 cases from the literature, including one of their own. Davenport,8 in 1928, reported references to 734 cases in the world literature. The reports of surgical repair of LVFWR started appearing in the literature around 1970. 9-11 Raitt et al 12 in their publication in 1993 tabulated 72 long-term survivors of myocardial free wall rupture treated by surgery. Lateef et al./Ventricular free wall rupture Incidence The incidence of LVFWR is difficult to compute because the denominators used in different studies were dissimilar. Some studies might not have utilised the appropriate denominator. For example, scientific papers based on autopsy studies presented the data as the number of VFWR expressed as a percentage of the total number of autopsies. This kind of data would give the prevalence of VFWR among those who died of myocardial infarction (MI), but would not tell the frequency of the complication in patients suffering from acute MI. Incidence of myocardial rupture in published autopsy series of MI varied from 5.0% to 24.0%.13-35 Some studies utilised the cohort of patients with MI and cardiogenic shock (CS). In this selected group of patients, the incidence of VFWR varied between 2.7% to 10.5%.11,36 Figueras et al encountered 81 (5.4%) patients with VFWR among 1,487 patients with first MI, with Killip I and II status.37 In studies where the cohorts were smaller, even without selectivity (e.g. CS, Killip classification), the incidence of VFWR was high viz., from 2.4% to 6.6% 38-42 with the exception of the study by Park et al, where in a small cohort the rate was less than 1.0%.43 An earlier exception to this was a population-based study with high (95%) autopsy rate from Sweden. 44 In this study there were 2,477 "attacks" (i.e. MI) of which 858 were fatal. One hundred and four (4.2%) of them had cardiac rupture and haemopericardium. Considering the apparently high mortality rate (34.6%), one may suspect that the total number of MI patients was actually more than 2,477 or that Swedes were more likely to develop VFWR. When studies with a large cohort of MI patients were evaluated for the frequency of VFWR, the incidence seemed to be around 1.0%. 45-47 Colletti et al found that LVFWR contributed to about 24.0 % in hospital mortality after acute MI and it was present in 40.0% of patients who died of acute MI in the first week.48 It is evident that the incidence of VFWR is not well defined in its scope. There is a suggestion that it may be increasing as a cause of death among victims with MI. This increase may be more apparent than real as other causes of death have become less common. 49-52 In a study from 239 Vienna, the rate of myocardial rupture was unchanged over a recent 16-year period.53 A reasonable estimate of the incidence of LVFWR after MI seems to be closer to 1.0%. 54 The often-quoted figure of annual death rate of 25,000 persons in the USA from cardiorhexis (myocardial rupture) comes from the article by Bates et al. 55 There was, however, no mention as to how this figure was arrived at. Risk factors T h e t y p i c a l p a t i e n t w i t h LV F W R i s u s u a l l y described as an older female, with no previous MI, no left ventricular hypertrophy, who has never experienced myocardial ischaemic symptoms or had only minor symptoms previously and who has acute transmural myocardial infarction, without mural thrombus. In the Thrombolysis and thrombin Inhibition in Myocardial Infarction (TIMI) 9A and 9B trial, the patients with VFWR were of lower body weight and smaller stature. 54 When age and other covariates were taken into consideration as independent variables, females were not markedly more at risk than males of the same age. The odds ratio for females to have cardiac rupture, adjusted for age and other covariates, drops from the unadjusted ratio of 2.41 to 1.62. 46 Chandra et al showed that women, age for age, had higher mortality from all causes after MI. 48 Weaver et al found that after a d j u s t i n g f o r a l l t h e d i f f e re n c e s i n b a s e l i n e characteristics, known to be important for prognosis, there was a slight excess in the risk of mortality for women (relative risk=1.15) after MI. 56 Patients with VFWR (or tamponade presumed to be from rupture) usually have significantly less prior history of MI or angina.36,55,57 Often, VFWR is a complication of first MI.34,57 These patients are less likely to have diabetes mellitus and peripheral vascular disease, 36,54 both conditions are associated with the development of collateral circulation, which is thought to decrease the likelihood of rupture. 36 (Table 1) However, it is likely that diabetes mellitus has neither a protective nor a deleterious effect on VFWR. 58 It is also possible that diabetics tend to present late because of absence of pain or atypical pain symptoms.59 240 Table 1. Factors indicating increased risk for VFWR Demographics Older age Female Coronary risk factors Non-diabetic Hypertension Vascular risk factors First myocardial infarction No peripheral vascular disease No left ventricular hypertrophy No history or only a very recent history of angina Patient factors Low body weight/small stature Within 5 days of MI Recurrent chest pain with no ECG changes suggestive of re-infarction or infarct extension The role of hypertension as an etiologic factor is controversial. Some authors found enough evidence to blame hypertension for facilitating rupture.16,18,26,30,34,54,60 Recent literature, which included prospective studies, showed a similar incidence of hypertension among those with or without rupture. 17,32,33,35,36,42,51,52,57 Figueras et al noted that hypertension at presentation after MI, was seen in those patients who had early rupture, but not in those who had late rupture. 61 Exertion, documented as such or presumptively so, by late presentation to hospital after the infarction (presuming that hospital admission would have rendered them with bed rest), seemed to increase the incidence of VFWR. 18,62 Solodky et al in a stepwise logistic regression model, found that advanced age, female gender, Killip class >1, tachycardia (>100 beats/ min), hypotension on admission and the use of thrombolytics to be independently associated with cardiac rupture. The more the number of these adverse variables present in a patient, the greater was the risk of cardiac rupture.39 A retrospective study from Portugal showed no difference in incidence of cardiac rupture with or without thrombolysis. 63 Nakamura et al detected a slight advantage (1.7% Vs 2.7%) in favour of thrombolysis. 64 Early thrombolytic therapy appeared to improve survival and decreased the risk of cardiac Hong Kong j. emerg. med. Vol. 10(4) Oct 2003 rupture. 65,66 One other group of agents used in the treatment of MI is nitrates. In a case controlled retrospective study, Pollak et al showed a beneficial effect of administration of nitrates, intravenously or orally, on the incidence of VFWR. 67 Pathology A patient with myocardial rupture is more likely to have the culprit infarction as her first infarction. After the MI, the weakened infarcted segment of cardiac muscle gives way under the strain of intraventricular pressure and the pressure gradient created. Thus, if there is a septal infarct, left to right pressure gradient could cause ventricular septal perforation. Intraventricular pressure is always more than intrapericardial pressure. However, in terms of pressure gradient, the right ventricle is not subject to strain comparable to the left ventricle, and hence the much lower frequency of right ventricular rupture. This is not the only factor which protects the right ventricle. The right ventricle has better collateral circulation and also thinner wall, allowing better perfusion of myocardium and decreasing the likelihood of transmural infarction. Myocardial free wall rupture of atrial chambers has not been reported. Between the two ventricles, the left is almost always the one that ruptures. Right ventricular free wall rupture is rare, as exemplified by the first case of Cobbs et al, 10 three in the study by Lopez-Sendon et al38 and one by Sherer et al.68 Anterior and lateral wall ruptures of the left ventricle are much more prevalent than posterior wall ruptures, probably because of the protection afforded by the adherent pericardium. The rupture is consistently in the infarcted area, somewhat eccentrically located and often near the junction of infarcted and viable myocardium.55,69 The sites are categorised according to whether it is near the atrioventricular groove (basal), near the apex (apical) or in between (middle) and whether it is on the anterior, lateral or inferior surface. Thus, there are nine different sites, i.e. anterior basal, lateral basal, inferior basal, anterior middle, lateral middle, inferior middle, anterior apical, lateral apical and inferior apical. (Table 2) Out of these possible Lateef et al./Ventricular free wall rupture 241 Table 2. Sites of VFWR and their frequencies haemopericardium and cardiogenic shock leading quickly to death.42,80-82 Subacute or stuttering ruptures imply gradual or incomplete ruptures of the infarcted area with slow and/or repetitive bleeding in the pericardial sac causing progressive or recurrent cardiac tamponade producing waxing and waning of symptoms and signs indicating haemodynamic instability. The chronic course is where there is d e v e l o p m e n t o f ve n t r i c u l a r p s e u d o a n e u r y s m detected at surgery or autopsy. This is generally asymptomatic. 83 Positions Basal Middle Apical Anterior ++ +++ ++ Inferior + ++ + Lateral ++ +++ ++ +++ indicates the most common type + indicates the least common type rupture sites, the anterior and lateral middle sites together made up 58% of all ruptures.69 In the study by Batts et al, 66% of the rupture sites were in the middle location and 48% of the total were in anterior and lateral middle sites. 34 (Table 2) Although interventricular septal rupture and ventricular free wall rupture are two distinct anatomical entities, there are patients who suffer both ruptures simultaneously.70 Purcaro et al described six pathologic types of ruptures encountered in their series of 28 patients.42 They were: (1) through and through straight rupture of normal thickness myocardium (Perdigao71 Type I); (2) similar b u t t h r o u g h t h e t h i n n e c r o t i c m y o c a rd i u m ; (3) multiple small perforations (Perdigao Type II); (4) rupture of outer layer only (Perdigao Type IV); (5) subepicardial haematoma without free rupture into the pericardial sac; and (6) haemorrhagic infarct with wall integrity but leaking surface. Their classification covers all the cases described in the literature except type III of Perdigao et al in which the orifice of rupture is protected either by thrombus on the ventricular side or by pericardial symphysis.71 The size of the rupture varied from not detectable (leaking surface) 42 to 70 mm. 55 Some studies found that larger infarcts were more prone to LVFWR.27,55,57 Others reported that smaller infarcts were often found in association with LVFWR. 12,17,33,72,73 Extensive coronary artery disease was noted by Bates et al55 but most of the authors found that the disease was limited to only one vessel.15,17,32,71,73-79 Clinical features Clinically, there are acute, subacute and chronic VFWR. Acute or blow out rupture is a sudden transmural rupture of the infarcted area causing VFWR occurs within twenty-four hours of MI in 20.0% to 30.0% of those who eventually rupture in any given series30,41 and within one week in 80.0% to 100.0%.34,41,57 Only the series by Purcaro et al showed a substantially higher incidence of VFWR (53.6%) on the first day.42 Ventricular free wall rupture should be suspected when a patient recovering from acute myocardial infarction experiences chest pain and cardiovascular collapse. 79 Rupture may occur in patients doing well after their first MI. Acute electromechanical dissociation (EMD) is a specific and very suggestive sign of VFWR in a patient with first MI without cardiac failure.35 This criterion alone, however, may still be due to other possible diagnoses such as massive pulmonar y embolism post-MI. In practical terms, no harm is likely to be done by this mistake, as these misdiagnosed patients are likely to have massive MI not amenable to any treatment. The association of bradycardia, distended neck veins, and cyanosis of head and neck has also been noted as a significant manifestation. Lopez-Sendon et al on a prospective study of more than 1,400 patients concluded that of all variables studied, hypotension, haemodynamic cardiac tamponade, pericardial effusion >5 mm at end-diastole on echocardiogram, echocardiographic abnormalities of haemopericardium and cardiac tamponade taken together have high predictive value.38 Hypotension as such is not diagnostic but the fact that every patient who developed VFWR has hypotension makes it imperative to use other studies to exclude VFWR. Symptoms distinct from the initial chest pain and other symptoms of acute MI were present consistently in patients who subsequently developed LVFWR. 42 Presence of at least two out of three symptoms from a symptom triad of (1) positional pleuritic chest pain 242 with or without a rub or recurrent uncharacterised chest pain; (2) single or repetitive large volume unprovoked emesis; and (3) unexplained restlessness or agitation, was consistently noted in 84% of patients.69 Physical examination will reveal evidence of hypoperfusion of organs. Signs of pericardial tamponade will be evident to a variable extent but classical signs may not always be present. Unconsciousness and agonal respiration will be a manifestation of reduced brain perfusion. Patients with subacute rupture may show improvement in between hypotensive episodes. Investigations Patients who are prone to develop VFWR may show certain characteristic findings on their electrocardiogram (ECG). In one study, deviation of ST segment or T wave or both, from expected evolutionary pattern during the first 72 hours after onset of MI, was observed consistently in all patients. 69 In another study, sinus tachycardia defined as a regular rate over 100/min was noted on the admission ECG of all patients who eventually developed LVFWR. If there was inferior wall MI leading to LVFWR, then the sum total of ST-segment deviation in all 12 leads was significantly higher in those with rupture. Other ECG findings noted with anterior and inferior wall rupture following MI were R wave duration of 20 ms in aVR84 and ST-elevation ≥0.1 mV in Lead II. With inferior wall MI, in addition to tachycardia (>100/min), there were R wave duration >20 ms in aVR and V6; ST elevation ≥0.1 mV in leads II, aVF, V4 to V6; and T wave negativity in leads II, III, aVF and aVR. Combined criteria of tachycardia and ST elevation in V5 for inferior MI were useful predictors of inferior wall rupture with 92% specificity. 85 The combined criteria of tachycardia and ST elevation in lead II were useful predictors of anterior wall rupture with 58% specificity. 85 Yoshino et al also observed that ST elevation in lead aVL in acute anterior MI was the only independent predictor of VFWR (odds ratio 12.1).85 In the study by Figueras et al, patients with anterior acute MI who had high ST elevation (6-7 mm) on the admission ECG were at higher risk of LVFWR.61 Sudden increase in amplitude of T wave or reversal to upright of previously inverted T wave is highly Hong Kong j. emerg. med. Vol. 10(4) Oct 2003 suggestive of haemopericardium and hence of VFWR. Mir described an ECG finding of a monophasic RS complex with an upright T wave and progressive ST segment elevation, called an "M complex" which was seen in patients who went on to develop VFWR. 86 Notwithstanding the findings of these authors, Purcaro et al in their prospective study attached so little importance to ECG findings that it was not even mentioned. In the discussion, they concluded that the ECG findings of rupture were confusing.42 Other studies drew similar conclusions that none of the ECG findings were sensitive or specific or pathognomonic for predicting cardiac rupture.12,38,81 Abrupt transient hypotension and bradycardia followed by EMD are invariably the signs of bleeding into the pericardial sac. Sudden EMD without overt heart failure in a patient with the first MI has a predictive accuracy of 97.6% for the diagnosis of VFWR. 35 The haemopericardium causes pericardial tamponade and associated manifestations such as cyanosis, jugular venous distension and altered sensorium. This may be a terminal event but occasionally the patient may improve spontaneously, transiently or even permanently. Where there is a high clinical suspicion of VFWR and conditions permit, an echocardiogram should be performed. Echocardiography is the best way to confirm the diagnosis. Presence of liquid in the pericardial sac especially with evidence of solid clot by high acoustic intrapericardial echoes together with diastolic compression of the right ventricle is diagnostic. If the leak into the pericardial cavity is demonstrated, the diagnosis is confirmed beyond any doubt. Cardiac catheterisation is an unwarranted procedure. It can be performed later if indicated. 42,81 If a SwanGanz catheter happens to be already inserted, the multiple level pressure measurements show the diastolic equalisation of right atrial, pulmonary artery, and pulmonary capillary wedge pressures. Other findings include right atrial pressure with deep x descent and a shallow y descent, decrease in the pulse pressure in the pulmonary artery, inspiratory elevation of right atrial pressure and pulsus paradoxus. Pericardiocentesis with aspiration of fluid, especially blood, clinches the diagnosis and also alleviates the adverse pathophysiology of tamponade. However, negative pericardiocentesis does not exclude VFWR. Lateef et al./Ventricular free wall rupture Treatment The treatment of subacute cardiac free wall rupture is surgical irrespective of the clinical status of the patient. 11,12,38,42,43,48,52,57,79-82,87 Acute or blow out rupture is generally not amenable to surgery because the course of events is so rapid that it is not feasible in most institutions to take these patients to a surgical suite in time to undergo surgery. McMullan et al believe that EMD is a diagnostic sign and should be followed by an echocardiogram if available and feasible. In the event of progression to cardiogenic shock or cardiorespiratory arrest, immediate surgery is warranted. 82 The mortality rate for surgery in acute ruptures is high but the mortality rate without surgery is virtually 100%.12,49,55 As time is of the essence and diagnostic certainty might not be possible, surgery is sometimes justified on the basis of a strong clinical suspicion. This is especially so as there have been no reported operative deaths in patients who were explored but found not to have myocardial rupture.12,38 The operation should preferably be done in a hospital which has full facilities for cardiopulmonary bypass. In hospitals with no facility for cardiopulmonary bypass, patients with anterior or lateral infarction may still have a chance of survival because these ruptures can be repaired with sutures buttressed with felt, without cardiopulmonary bypass. 4 Temporising with modalities such as administration of inotropes and fluids, pericardiocentesis, intra-aortic balloon pump insertion or even bedside cardiopulmonary resuscitation wastes valuable time in a patient with acute rupture. Even in subacute rupture (stuttering rupture), cardiac catheterisation is not indicated. 11,12,42,45,81,82 It can be performed later if indicated. After categorically stating that the treatment of VFWR is surgical, it should be pointed out that there are more than occasional descriptions of patients who survived the non-operative treatment, sometimes even with no specific treatment. 36,37,40,68,88 If, for any reason, a decision is made to treat a patient medically and for those patients awaiting surgery, the first objective is to obtain and maintain haemodynamic stability. This is best achieved by rapid infusion of fluids and inotropic support. Pericardiocentesis if successful may 243 help to relieve the impact of tamponade. Intra-aortic balloon pump is an adjunct worth considering under appropriate circumstances. Pharmacological afterload reduction may also be considered. Prognosis Dramatic as the presentation and treatment of LVFWR is, surgery would not be justified if the results were not correspondingly dramatic. Acute LVFWR usually results in death within 30 minutes of cardiovascular collapse and hence it is unlikely to be amenable to surgery. If surgery can be performed before death, the occasional survivor is worth the effort. Subacute rupture is a different issue. Padro et al had 100% long-term survival rate after surgery. 81 No other group had shown such remarkable results, but the results were still encouraging, e.g. 48.5% longterm survivors from the series by Lopez-Sendon et al.38 Purcaro et al had 16 out of 24 surgically operated patients discharged well from the hospital. Eleven (45.8%) of these were living normal lives at home. 42 These were three series with relatively large number of patients. One multicenter, multinational study had 38% survival.36 For a small number of operations, Park et al had four out of four survivors. 43 McMullan et al had also successfully operated on acute (blow out) LVFWR with long-term survival.82 Other centres with only small numbers of patients have also shown remarkable successes with long-term survival after surgery. 10,11,12,87,89-95 Summary VFWR is a catastrophic complication that occurs within 7 days, in 1-4% of patients with acute MI. It can manifest as cardiogenic shock or circulatory collapse. It often occurs in older females with their first, small, transmural acute MI. Acute onset of shortness of breath, cardiac arrest, shock, diaphoresis, unexplained emesis or syncope may herald the onset of VFWR. A high index of suspicion is essential. 244 Resuscitation with fluid, cautious use of inotropes and pericardiocentesis can only offer temporary support at best. Without prompt surgical repair, mortality remains very high. References 1. 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