WBR0480

Author	[[PageAuthor::Ayokunle Olubaniyi, M.B,B.S [1]]]
Exam Type	ExamType::USMLE Step 3
Main Category	MainCategory::Inpatient Facilities
Sub Category	SubCategory::Cardiovascular
Prompt	[[Prompt::A 66 year-old woman was admitted following an acute ST segment elevation myocardial infarction. She subsequently had percutaneous coronary intervention done where a thrombus was found causing an 80% occlusion of the proximal one-third of the left anterior descending artery (LAD). The interventional cardiologist was very happy to have achieved a 100% reperfusion in the epicardial artery (TIMI grade 0), but the patient continued to experience a sharp chest pain and the ST-segment elevation on the EKG failed to resolve in the absence of a mechanical occlusion. It was later postulated that the symptoms failed to resolve due to non-perfusion of the myocardium. Which of the following best describes the pathophysiology of the most likely cause of the patient’s persistent chest pain?]]
Answer A	AnswerA::Ischemic preconditioning
Answer A Explanation	[[AnswerAExp::Ischemic preconditioning – This is an intrinsic process in the heart whereby short episodes of ischemia protects the heart from subsequent ischemic insults. It has been shown to prevent against myocardial necrosis. Consequently, the presence of pre-infarction angina has been shown to preserve collateral circulation after myocardial infarction.]]
Answer B	AnswerB::Distal embolization of atheromatous plaques
Answer B Explanation	AnswerBExp::Distal embolization of atheromatous plaques is the primary mechanism explaining the pathogenesis of the no-reflow phenomenon
Answer C	AnswerC::No-reflow phenomenon
Answer C Explanation	AnswerCExp::This refers to the condition itself and not the pathophysiologic mechanism.
Answer D	AnswerD::Reperfusion injury
Answer D Explanation	[[AnswerDExp::Reperfusion injury from the release of oxygen free radicals during inflammation and temporary occlusion of blood flow has also been postulate. This is however not the best most appropriate answer choice]]
Answer E	AnswerE::Coronary vasoconstriction
Answer E Explanation	[[AnswerEExp::Vasoconstriction secondary to serotonin, adenosine diphosphate, thromboxane A2, released by the embolized platelet-rich atheromatous material is a possible mechanism for the development of no-reflow phenomenon but this is not the main mechanism of its etiology.]]
Right Answer	RightAnswer::B
Explanation	[[Explanation::The failure to achieve myocardial reperfusion despite the restoration of a normal epicardial coronary blood flow in the absence of any mechanical occlusion is known as No-reflow phenomenon. Several pathophysiologic mechanisms play regarding its etiology including microvascular damage, myocardial necrosis, coronary vasoconstriction, reperfusion injury. The main pathophysilogic mechanism implicated is the distal embolization of atheromatous plaques or thrombi. During PCI, microthrombi and small particles of plaques are thought to be showered downstream, occluding small arteries, arterioles, and collateral microvasculature. This is usually observed as either the failure of resolution of the presenting cardiac symptoms or the presenting EKG findings. The patients can also be hypotensive requiring inotropic support, temporary cardiac pacing or intraortic balloon pump. The treatment of mainly pharmacologic with medications such as vasodilators (verapamil, adenosine, nitroprusside) through the intracoronary route. No-reflow phenomenon has been shown to be an important predictor of mortality in this patients. Educational Objective: Distal embolization of atheromatous plaques is the primary mechanism explaining the pathogenesis of the no-reflow phenomenon References: http://www.wikidoc.org/index.php/No-reflow_phenomenon]]
Approved	Approved::Yes
Keyword	WBRKeyword::No-reflow phenomenon, WBRKeyword::PCI complication
Linked Question	Linked::
Order in Linked Questions	LinkedOrder::