Cardiac rupture

Patients with seropositive rheumatoid arthritis taking long-term systemic glucocorticoids are at risk of accelerated cardiac rupture in the setting of transmural acute myocardial infarction treated with thrombolytic drugs (25). 

Increased risk of reinfarction, cardiac rupture, or arrhythmias, but impact of complete revascularization on risk is unknown... 

Heymans S, Luttun A, Nuyens D, Theilmeier G, Creemers E, Moons L, et al. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. Nat Med 1999 5 1135-1142. 

Early use within 6 hours (or at most 12 h) of onset (i.v. for 24 h then oral for 3-4 weeks). Benefit has been demonstrated only for atenolol. Cardiac work is reduced, resulting in a reduction in infarct size by up to 25% and protection against cardiac rupture. 

In addition to thrombolysis and aspirin, a third treatment has been shown to reduce mortality in MI, namely P-blockade. In the ISIS-1 study, atenolol 50 mg was given i.v. followed by the same dose orally. The reduction in mortality is due mainly to prevention of cardiac rupture, which appears interestingly to remain the only complication of MI that is not reduced by thrombolysis. The usual contraindications to P-blockade apply, but most patients with a first MI should be able to receive this treatment. 

The most important mechanical complications of ACS evolving to MI occur in transmural infarctions, usually Q-wave infarction. They consist in cardiac rupture, which may occur in the free wall, the interventricular septum or the papillary muscles and the ventricular aneurisms. 

Cardiac ruptures are much less frequent with the currently available therapies. However, they may still be found in 2-3% of Q-wave infarctions and are still an important cause of mortality in the acute phase (Figueras et al, 1995). Additionally, cardiac rupture may occur without prodromal signs in patients with evolving Q-wave or equivalent infarction, sometimes small and for that their occurrence is even more dramatic. Therefore, it is extremely important to assess correctly the subtle premonitory data, such as some electrocardiographic details. Contrary to what occurs in primary VF, which may be virtually always resolved in the coronary care unit, cardiac rupture requires urgent surgical treatment. The mortality rate is only below that of cardiogenic shock secondary to a massive infarction. Fortunately, also the latter is much less frequent with the currently available therapies. 

Figure 8.34 Patient of 68 years of age who suffered sudden death 10 days after an acute infarction. A progressive depression of the automatism (with the appearance of a slow escape rhythm) is shown in the Holter ECG recording, until cardiac arrest occurs, due to an electromechanical dissociation caused by cardiac rupture.

From the prognostic point of view, these usually correspond to large anteroseptal or inferolateral infarctions. In case of acute inferior MI the presence of PR-segment depression >1.2 mm in inferior leads has been demonstrated to be a marker of higher risk of in-hospital mortality and cardiac rupture (Jim et al., 2006) (Figure 10.6). Often these cases present supraventricular arrhythmias, especially atrial fibrillation. 

Oliva PS, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarc-... 

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