Concomitant acute myocardial infarction and ischemic cerebrovascular strokes has been rarely reported in the literature [1]. In this report, after the patient has developed acute transmural infero-posterior and right ventricular infarction he suddenly developed a rapid onset and a progressive course of worsening of his conscious level with an NIHSS >25 [2] denoting severe ischemia. This was later confirmed by computed tomography of the brain which revealed massive cerebral and brainstem infarction. We suggest that there is a certain relationship connecting both pathologies together and not just a mere association. We assume that the following mechanisms may explain the occurrence of an ischemic cerebrovascular stroke immediately after an acute inferior and right ventricular infarction.
1- If the underlying pathological mechanism for this transmural myocardial infarction is dissection of the ascending aorta extending to the right coronary ostia, then an extension of the dissection process to involve the vertebral artery which can further extend to involve the basilar artery can explain the association of both events. In our case, the affection of the brain-stem, both cerebellar hemispheres and both occipital lobes indicates that the basilar artery is the culprit vessel for his CNS manifestations.
2- Patients with right ventricular infarction especially those with severely impaired right ventricular function can be complicated with the development of a right ventricular thrombus. In approximately 20% of the population, the foramen ovale fails to seal entirely [3]. A patent foramen ovale (PFO) in a patient with right ventricular failure and subsequent elevation of right sided pressure can be a cause for paradoxical embolism after development of right ventricular thrombus.
3- The sudden development of severe hypotension in patients with long standing hypertension and initial failure of the auto-regulatory mechanisms can lead to sudden reduction in the cerebral blood flow and subsequent infarction. This is especially evident in the brainstem more than the rest of the brain where there is relative inability of the brainstem circulation to auto-regulate intravascular pressures. In the Systolic Hypertension in the Elderly Program (SHEP), which demonstrated an overall benefit of antihypertensive therapy in the prevention of strokes [4], lowering of diastolic blood pressure to less than 60 mm Hg was paradoxically associated with an increased risk of stroke [5]. Severe hypotension may complicate acute right ventricular infarction and can explain this massive cerebral infarction.
4. Ischemia at a distance is another possibility that can explain the left ventricular systolic dysfunction present in this patient despite a small infarction. In a patient with a previously atherosclerotic left anterior descending artery and is dependant mainly on the right coronary artery as a source of collateral circulation supplying the left ventricle; if the RCA is totally occluded, then this will dramatically affect the left ventricular function. Left ventricular systolic dysfunction can be complicated by the formation of a left ventricular thrombus and subsequent embolization. In our patient, the preserved R waves in the precordial leads suggest a previously non-infarcted left ventricle. The only possible explanation for the left ventricular dysfunction on the echocardiogram is "ischemia at a distance".
Due to the rapid downhill course of the disease process in our patient, we could not radiologically confirm the exact underlying pathophysiologic mechanism explaining this association. However, the absence of echocardiographic evidence of a right or left ventricular thrombus and PFO makes thrombo-embolism a remote possibility. Also, the diameter of a patent foramen ovale is usually small which will not permit the passage of a large thrombus sufficient to cause a large infarction as described in the case. Therefore we assume that the most likely explanation to the concomitant cardiac and cerebral infarction in our case is either a dissection that first obstructs the right coronary artery followed subsequently by its extension and obstruction of the basilar artery, or that severe stenosis in the vertobro-basilar territory existed prior to the present episode, and a furthur decrease of blood flow in this area following a marked reduction of blood pressure after right ventricular infarction resulted in the development of massive cerebral infarction.
This case was such a complicated one that carried an unfavorable prognosis as it comprised two pathologies both of which can be life-threatening. The report aims only to provide possible explanations for this cardio-cerebral infarction and to sensitize readers to this association which needs further research. The lack of guidelines that describe the ideal management strategies further complicates the situation. Whether Alteplase therapy is beneficial for concomitant acute myocardial infarction and acute ischemic stroke should be studied. Further studies are also warranted to determine whether it is better to close the PFO or not in patients with high risk of thrombo-embolic complications.
