Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptomatic common carotid artery occlusion (CCAO) is rare. We studied 17 patients with ischemic cerebrovascular symptoms and unilateral CCAO on angiography to help clarify clinical and radiologic features. Mean age was 62 years; 65% were women. Predominant symptoms and signs included visual-ipsilateral monocular or retrochiasmal symptoms (88%), motor weakness (88%), sensory disturbance (59%), dizziness/lightheadedness (53%), and syncope (24%). Dysarthria, headache, or involuntary limb shaking occurred less frequently. Positionally related symptoms occurred in approximately two-thirds of the patients. TIAs were often multiple and preceded a stroke or occurred without subsequent stroke in 82%. Hemispheric TIAs contralateral to the CCAO occurred in 41%. Ten patients (59%) suffered stroke, seven (70%) of which were ipsilateral to the CCAO. Vascular risk factors included cigarette use (76%), hypertension (71%), diabetes mellitus (41%), and hyperlipidemia (41%); 82% had two or more risk factors. Known cardiac disease was present in 59%. CCAO was present at the origin of the vessel in most patients. Most had atherosclerotic narrowing of multiple extracranial large vessels. During follow-up, none of the patients had a spontaneous second infarct; five had TIAs, including two with amaurosis fugax, all in the CCAO territory. More restricted external carotid collaterals may, in part, explain the higher frequency of ipsilateral stroke and contralateral TIAs than reported for internal carotid occlusion.
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PMID:Common carotid artery occlusion. 279 68

Myocardial infarctions are frequently complicated by tachyarrhythmias, which commonly have wide QRS complexes (QRS duration > 120 milliseconds). Many published criteria exist to help differentiate between ventricular and supraventricular mechanisms. We present a case of a 61-year-old male with a history of hypertension, hyperlipidemia and coronary artery disease with prior stenting of the right coronary artery (RCA). He had been noncompliant with his antiplatelet medication and presented with cardiac arrest secondary to in-stent thrombosis. He was resuscitated and his RCA was re-stented, after which he made a good neurological recovery. During cardiac rehabilitation several weeks post-intervention, he was noted to have sustained tachycardia with associated nausea and lightheadedness, but no palpitation symptoms, chest pain or loss of consciousness. He was sent to the emergency department, where his electrocardiogram showed a tachycardia at 173 beats per minute which was regular, with a relatively narrow QRS duration (maximum of 115-120 msec in leads I and AVL) with a slurred QRS upstroke. This morphology was significantly different from his QRS complex during sinus rhythm. Intravenous diltiazem was ineffective but an amiodarone bolus terminated the tachycardia. The patient was admitted to the coronary care unit and treated with intravenous amiodarone infusion. A subsequent electrophysiology study was performed, showing inducibility of the clinical tachycardia. Atrioventricular (AV) dissociation was present during the induced arrhythmia, confirming the diagnosis of ventricular tachycardia. An implantable cardiac defibrillator was placed and the patient was discharged.
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PMID:Narrow Complex Ventricular Tachycardia. 2887 96

Mitral valve prolapse (MVP) is characterized by typical fibromyxomatous changes in the mitral leaflet tissue with superior displacement of one or both leaflets into the left atrium. An echocardiogram is a fundamental study required for the diagnosis of MVP with a flail leaflet and grading of mitral regurgitation (MR) severity. Most patients with MVP have a risk of cardiovascular morbidity and mortality similar to that of the general population, though moderate to severe MR and left ventricular (LV) ejection fraction less than 50% have been postulated to increase the risk of adverse cardiac events. In this case report, we present an isolated flailed P3 scallop of the mitral valve leaflet leading to severe MR and acute congestive heart failure. A 54-year-old African-American male with a medical history of hypertension, hyperlipidemia, and transient ischemic attack, presented to the emergency department (ED) for evaluation of dyspnea on exertion. The patient reported that his dyspnea started one week prior to ED visit and was associated with intermittent chest pain. He also endorsed mild orthopnea and lightheadedness, though he denied any syncopal event. Vital signs were found within normal limits on arrival. He clinically appeared to be volume overloaded which improved quickly with IV furosemide. Transesophageal echocardiogram (TEE) with 3D image acquisition showed significant for hyper-dynamic LV function and evidence of isolated flailed P3 scallop of the mitral valve (MV) leaflet resulting in a severe eccentric, anteriorly directed MR jet. The MV leaflets did not appear thickened, and there was no evidence of mitral or aortic stenosis. Cardiac catheterization showed multivessel disease for which the patient underwent coronary artery bypass grafting and MV repair. This patient presented with new-onset congestive heart failure secondary to severe MR associated with undiagnosed MVP. Commonly, the middle scallop (P2) of the posterior leaflet is more prone to prolapse due to its redundancy and variable thickness with the impact of greater systolic pressure. However, in this case of acute severe MR, we identified an isolated flail of the P3 segment. We believe that this rare TEE finding was associated with a torn chordae or ruptured papillary muscle secondary to ischemic disease as the posteromedial papillary muscle has a single blood supply and is particularly prompted to injury from myocardial infarction.
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PMID:Isolated Flailed P3 Scallop of the Mitral Valve Leaflet in the Setting of Newly Diagnosed Heart Failure With Preserved Ejection Fraction. 3296 80

Medications for opioid use disorder (MOUD) and opioid agonist therapy (OAT) are the mainstays of treatment in opioid use disorder. Significant caution is encouraged upon initiation to reduce the precipitation of opioid withdrawal. Cardiac events in the setting of opioid withdrawal are rare and incompletely understood. A 46-year-old woman with a history of opioid-use disorder, hypertension, hyperlipidemia, diabetes, tobacco-use disorder, and rheumatoid arthritis presented with nausea, vomiting, and lightheadedness after taking naltrexone following buprenorphine. She was found to be hypertensive and tachycardic in the emergency department, with a troponin of 0.38 ng/mL (reference: 0.00-0.30 ng/mL) and an electrocardiogram (ECG) without ST or T-wave changes. She was admitted for a non-ST-elevation myocardial infarction (NSTEMI) and hypertensive emergency in the setting of opioid withdrawal. Her blood pressure was controlled, and she received full-dose aspirin and high intensity atorvastatin. Afterwards she was started on a modified OAT regimen of buprenorphine 8 mg daily. Her cardiac enzymes down-trended and her condition became stable after which she was discharged home. Cardiac events are an uncommon yet lethal occurrence in opioid withdrawal. The likely etiology of NSTEMI in our patient was demand ischemia induced by opioid withdrawal, augmented by her various other cardiac risk factors. Practitioners should be aware of these possible adverse events, especially in those with preexisting cardiac disease. Meticulous efforts should be made to instruct patients as to the proper dosing schedule when initiating opioid therapy, and when initiating MOUD/OAT in order to prevent poor outcomes.
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PMID:Naltrexone-Associated Non-ST-Elevated Myocardial Infarction. 3326 29