Two rare complications of myocardial infarction: a case report

Abstract

Background Mechanical complications following myocardial infarction (MI) have decreased in incidence due to the widespread use of early percutaneous coronary revascularization methods. We describe two rare complications as well as their natural history and uncertainties of the ideal management approach. Case summary Sixty-two-year-old female with multiple cardiovascular disease risk factors who had a delayed presentation of ST-segment elevation myocardial infarction and went on to develop dissecting intramyocardial haematoma progressing to ventricular septal rupture and coronary ventricular fistula. Discussion Intramyocardial haematoma is a rare complication of MI. It is considered to be part of the continuum of myocardial rupture which our patient eventually developed in the form of ventricular septal defect. The second rare entity in the same patient was development of a coronary ventricular fistula of the infarct-related stented, artery. The best way of managing dissecting intramyocardial haematoma is unclear with conflicting data between conservative and invasive strategies. Our patient failed the conservative approach as she progressed to frank myocardial rupture.

A new dimension to the STEMI-related mortality risk seen in the COVID-19 pandemic era

“…Delay between electrocardiographic documentation of STEMI and subsequent development of VSR ( Table 2 ). Twenty patients (13 male) belonged to this category [ [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] ]. Their mean age was 66.…”

“…Thirteen patients had multivessel disease. Two patients had coexisting left ventricular aneurysm [ 49 , 60 ], associated, in one patient, with non-fatal hemopericardium but without demonstrable left ventricular free wall rupture (LVFWR) [ 60 ]. Non-fatal hemopericardium was documented in one other patient who had neither left ventricular aneurysm nor demonstrable LVFWR [ 52 ].…”

“…Conversely, in the presence of severe hypotension, the systolic murmur of VSR “may be difficult to identify because turbulent flow across the defect is reduced” [ 61 ], and the same might also be true of the systolic murmur of PMR [ 62 ]. Clinicians should also be especially vigilant for “stepwise” evolution of VSR [ [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] ], whereby a patient with delayed presentation of STEMI initially presents without clinical or echocardiographic stigmata of VSR but subsequently experiences hypotension and/or increasing breathlessness signalling onset of VSR [ [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] ]. The onset of VSR, in such cases, is typically associated with new-onset pansystolic murmur.…”