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A 63 year old man with a history of hypertension, hyperlipidemia, prediabetes, and a family history of CAD developed chest pain, shortness of breath, and diaphoresis after consuming a large meal at noon. He called EMS, who arrived on scene about two hours after the onset of pain to find him hypertensive at 220 systolic. Murakami MM.
Vital signs were noted to be unremarkable with respect to any hypo-hypertensive crisis, hypoxia, etc. He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardialinfarction, or any prior PCI/stent. No appreciable skin pallor.
His father and brother both died of myocardialinfarction at ages 61 and 45, respectively. There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1]
As a brief review, HCM is a genetically inherited disorder that produces structural disarray in the myocardial cells. There is ventricular hypertrophy in the absence of abnormal loading conditions, such as aortic stenosis, or hypertension, for example – of which the most common variant is Asymmetric Septal Hypertrophy. 40; 1234-1241.
Diamond and Forrester accomplished this by first establishing the prevalence of coronary artery disease based on how clinically likely patients with chest pain symptoms were found to have coronary disease based on a coronaryangiogram. Women also had more cardiovascular risk factors, including hypertension (66.6%
Case submitted and written by Mazen El-Baba MD, with edits from Jesse McLaren and edits/comments by Smith and Grauer A 90-year old with a past medical history of atrial fibrillation, type-2 diabetes, hypertension, dyslipidemia, presented with acute onset chest/epigastric pain, nausea, and vomiting. Incidence of an acute coronary occlusion.
It was edited by Smith CASE : A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chest pain, weakness and nausea. The diagnostic coronaryangiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve.
The left and right coronary arteries were slender and narrow, which was relieved after the injection of 100g nitroglycerine through the left coronary artery. After performing a coronaryangiogram, the patient was given long-acting nitrates and calcium channel blockers orally, and her chest pain did not reoccur.
Angiogram Door to balloon time was 120 minutes (much too long) because of time taken for a CT. Coronaryangiogram showed 100% mid LAD occlusion for which she received a DES with excellent angiographic result. It was not SCAD (coronary dissection) Highest troponin I was 37,000 ng/L, but it was not measured to peak.
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