Myocardial Catastrophe

Abstract

A 44-year-old woman presented to her local emergency room with a 1-day history of nausea, fatigue, and fever of 101°F. At that time, she denied chest pain, dyspnea, cough, orthopnea, or lower-extremity edema. An ECG was reportedly normal, and she was treated with antiemetics and fluids and discharged home. The next day, she developed persistent, aching pain in her chest and jaw and presented to her primary care physician. Her medical history included obesity, depression, hyperlipidemia, and antiphospholipid antibody syndrome (APLAS) initially diagnosed in 1989 when she was 20 years of age complicated by 4 miscarriages, pulmonary emboli, and deep vein thrombosis for which she underwent inferior vena cava filter placement in 1997. She had experienced no thromboembolic events over the next 15 years. Her home medications were rivaroxaban 20 mg daily, aspirin 81 mg daily, furosemide 20 mg daily, simvastatin 20 mg daily, escitalopram 20 mg daily, and omeprazole 20 mg daily. She worked as a nurse and lived with her husband and 4 adopted children. She never smoked. Her mother carried the diagnosis of factor V Leiden. She was scheduled for an elective gastric bypass surgery in 2 days and had been instructed to hold her rivaroxaban for 4 days before surgery; therefore, she stopped anticoagulation 2 days before presentation.Dr Kirshenbaum: Her initial symptoms are quite nonspecific, with nausea and a low fever suggesting a viral process. However, the subsequent development of chest and jaw pain also raises the possibility of cardiac causes such as an acute coronary syndrome. Myocarditis also often presents with chest pain that can mimic an acute coronary syndrome and can be preceded by a viral prodrome. In addition, the recent discontinuation of rivaroxaban in a patient with a history of severe thrombophilia and APLAS is worrisome. Rivaroxaban carries a boxed warning that cautions that premature discontinuation of the drug increases the risk of thrombotic events and suggests coverage with another anticoagulant if clinically warranted.1 This patient had no bridging anticoagulation prescribed. Therefore, a new thrombotic event such as mesenteric ischemia or coronary thrombosis (epicardial or microvascular occlusion) must also be considered.Patient presentation (continued): Her chest pain led to a repeat evaluation in the same emergency room where she had presented the day before. At this point, her ECG had ST-segment elevations in the inferior and apical leads (Figure 1) that were new compared with her ECG 24 hours earlier. Her laboratory work at that time was notable for a troponin I level of 19 ng/mL. She was given aspirin, clopidogrel, and atorvastatin, started on unfractionated heparin; and transferred to a percutaneous coronary intervention-capable facility for cardiac catheterization.On arrival at the closest percutaneous coronary intervention-capable facility, she was afebrile and had a heart rate of 107 bpm, blood pressure of 105/74 mm Hg, respiratory rate of 24 breaths per minute, and oxygen saturation of 97% on 2 L...

Catastrophic antiphospholipid syndrome: challenging case and importance of multidisciplinary evaluation and management

“… 10 After cerebral involvement, cardiac effects of CAPS are noted to be the second most frequent cause of death. 11 Clinical deterioration has been seen in the form of worsening systolic dysfunction, 7 , 8 , 10 , 12 , 13 cardiogenic shock, 7 , 14 cardiac arrest, 12 and need for mechanical support. 12 , 14 …”

“… 11 Clinical deterioration has been seen in the form of worsening systolic dysfunction, 7 , 8 , 10 , 12 , 13 cardiogenic shock, 7 , 14 cardiac arrest, 12 and need for mechanical support. 12 , 14 …”

“…Target organ biopsy (renal in our case) showing ischemic microvascular injury of the kidneys, myocardium, or skin, as described previously, might have provided valuable insight into the underlying diagnosis. 6 , 12 , 14 , 15 However, the risks of withholding anticoagulation for biopsy after development of a splenic infarct was deemed too great. While large vessel vasculitis was considered, given the finding of aortitis, involvement of the glomerulus made this less likely.…”

Sudden Cardiac Arrest as the First Manifestation in a Patient with Catastrophic Antiphospholipid Syndrome

“…Regarding the etiology of CAPS-related acute cardiac failure, a number of different causes have been described, including macrovascular ( 4 ) or microvascular coronary artery embolization ( 5 ), valve involvement ( 6 ), fulminant myocarditis ( 7 ), and severe hypoxemia. In the present case, we failed to confirm the presence of microvascular coronary artery embolization or myocarditis since a cardiac biopsy or gadolinium-enhanced cardiac MRI could not be performed due to the patient's severe thrombocytopenia and kidney dysfunction.…”

Cardiac Magnetic Resonance in Rheumatology to Detect Cardiac Involvement Since Early and Pre-clinical Stages of the Autoimmune Diseases: A Narrative Review

“…LV dysfunction is a rare presentation ( 84 , 85 ) and the suspected mechanism identified in the autopsy is a widespread thrombosis of the intramyocardial arteries and arterioles ( 86 , 87 ), which one can assume leads initially to microvascular dysfunction, then microinfarctions of the myocardium generating small scars and fibrosis and finally compromising the ventricular function. Myocardial edema ( Figure 3b ) has ( 88 ) also been described as catastrophic ( 89 ).…”