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Managing Thrombosis and Hemorrhage in a Man with Myocardial Infarction and Traumatic Hemopericardium with Cardiac Tamponade.

ABSTRACT: A 79-year-old man had an out-of-hospital acute ST-segment-elevation myocardial infarction with cardiac arrest. Cardiopulmonary resuscitation performed by a bystander resulted in traumatic hemopericardium. We discuss the patient's case, highlight the challenges of managing simultaneously life-threatening thrombosis and hemorrhage, and present our conclusions regarding the patient's eventual death.

SUBMITTER: Bush AL

PROVIDER: S-EPMC8367290 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature

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Managing Thrombosis and Hemorrhage in a Man with Myocardial Infarction and Traumatic Hemopericardium with Cardiac Tamponade.

Bush Aaron L AL Allencherril Joseph J Alam Mahboob M

Texas Heart Institute journal 20210701 3

A 79-year-old man had an out-of-hospital acute ST-segment-elevation myocardial infarction with cardiac arrest. Cardiopulmonary resuscitation performed by a bystander resulted in traumatic hemopericardium. We discuss the patient's case, highlight the challenges of managing simultaneously life-threatening thrombosis and hemorrhage, and present our conclusions regarding the patient's eventual death. ...[more]

PMID: 34379771

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Project description:Cardiac dysfunction (CD) importantly contributes to mortality in trauma patients, who survive their initial injuries following successful hemostatic resuscitation. This poor outcome has been correlated with elevated biomarkers of myocardial injury, but the pathophysiology triggering this CD remains unknown. We investigated the pathophysiology of acute CD after trauma using a mouse model of trauma hemorrhage shock (THS)-induced CD with echocardiographic guidance of fluid resuscitation, to assess the THS impact on myocardial integrity and function. Mice were subjected to trauma (soft tissue and bone fracture) and different degrees of hemorrhage severity (pressure controlled ~MABP < 35 mmHg or <65 mmHg) for 1 h, to characterize the acute impact on cardiac function. In a second study, mice were subjected to trauma and hemorrhage (MABP < 35 mmHg) for 1 h, then underwent two echocardiographic-guided resuscitations to baseline stroke volume at 60 and 120 min, and were monitored up to 180 min to study the longer impact of THS following resuscitation. Naïve and sham animals were used as controls. At 60 min post-THS injury, animals showed a lower cardiac output (CO) and stroke volume (SV) and an early rise of heart fatty acid-binding protein (H-FABP = 167 ± 38 ng/ml; 90% increase from shams, 3.54 ± 3.06 ng/ml), when subjected to severe hemorrhage and injury. Despite resuscitation, these animals maintained lower CO (6 ml/min vs. 23 ml/min), lower SV (10 μl vs. 46 μl; both ~75% decreased), and higher H-FABP (levels (340 ± 115 ng/ml vs. 10.3 ± 0.2 ng/ml; all THS vs. shams, P < 0.001) at 180 min post-THS injury. Histopathological and flow-cytometry analysis of the heart confirmed an influx of circulatory leukocytes, compared to non-injured hearts. Myocardial injury was supported by an increase of troponin I and h-FABP and the widespread ultrastructural disorganization of the morphology of sarcomeres and mitochondria. DNA fragmentation and chromatin condensation driven by leakage of apoptosis-inducing factor (AIF) may suggest a mitochondria-driven progressive cell death. THS modeling in the mouse results in cardiomyocyte damage and reduced myocardial function, which mimics the cardiac dysfunction seen in trauma patients. This CD model may, therefore, provide further understanding to the mechanisms underlying CD and act as a tool for developing cardioprotective therapeutics to improve survival after injury.

Project description:BackgroundCoronary vasospasm is a rare cause of ST-segment elevation myocardial infarction (STEMI) and can be precipitated by numerous inciting factors including endogenous catecholamines. Differentiating coronary vasospasm from an acute atherothrombotic event is diagnostically challenging and requires a careful clinical history combined with electrocardiographic and angiographic abnormalities to make the diagnosis and guide therapy.Case summaryWe report a case of cardiogenic shock secondary to cardiac tamponade leading to an endogenous catecholamine surge resulting in profound arterial vasospasm and STEMI. The patient presented with chest pain and inferior ST segment elevations prompting emergent coronary angiography, demonstrating subtotal occlusion of the right coronary artery, severe proximal left anterior descending coronary artery stenosis, and diffusely stenosed aortoiliac vessels. Emergent transthoracic echocardiogram revealed a large pericardial effusion and hemodynamics consistent with cardiac tamponade. Pericardiocentesis resulted in dramatic hemodynamic improvement with immediate normalization of ST segments. Repeat coronary angiography performed one day later showed no angiographically significant coronary or peripheral arterial stenosis.DiscussionThis is the first reported case of simultaneous coronary and peripheral arterial vasospasm presenting as inferior STEMI caused by endogenous catecholamines from cardiac tamponade. Several clues suggest coronary vasospasm including the discordant electrocardiography (ECG) and coronary angiographic findings as well as diffusely stenosed aortoiliac vessels. Diffuse vasospasm was confirmed when repeat angiography performed after pericardiocentesis demonstrated angiographic resolution of coronary and peripheral arterial stenosis. Though rare, circulating endogenous catecholamines resulting in diffuse coronary vasospasm may present as STEMI and should be considered based on the clinical history, ECG findings, and coronary angiography.

Dataset Information

Managing Thrombosis and Hemorrhage in a Man with Myocardial Infarction and Traumatic Hemopericardium with Cardiac Tamponade.

Publications

Managing Thrombosis and Hemorrhage in a Man with Myocardial Infarction and Traumatic Hemopericardium with Cardiac Tamponade.

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