Thrombotic Thrombocytopenic Purpura Presenting as an Acute Coronary Syndrome

Introduction: Thrombotic thrombocytopenic purpura is a thrombotic microangiopathy caused by severely reduced activity of the von Willebrand factor-cleaving protease ADAMTS13. It is considered a medical emergency and could be fatal if appropriate medical management if not initiated in time. Rarely, it can present as an acute coronary syndrome. Case presentation: We present a case of an 80-year-old female with a past medical history of hypertension and irritable bowel syndrome who presented to the emergency department with chest pain. Her chest pain was centrally located, exertional and relieved by sublingual nitroglycerin. The patient also reported having dizziness, generalized fatigue and headache. On arrival, she was noted to be hypertensive but otherwise hemodynamically stable. Physical examination was unremarkable. Laboratory evaluation revealed elevated high sensitivity troponin with an initial value of 434 ng/L (reference range/L) and peaking at 817 ng/L, elevated creatinine at 1.61 mg/dL (reference range Discussion: Thrombotic thrombocytopenic purpura (TTP) is described by the classic pentad of microangiopathic hemolytic anemia, thrombocytopenia, renal involvement, central nervous system manifestations and fever. Our patient presented with chest pain and neurological symptoms and was found to have anemia, thrombocytopenia and elevated creatinine. Those findings with elevated troponin and EKG changes should raise the suspicion of TTP-related acute coronary syndrome. The exact mechanism of how TTP can cause acute coronary syndrome is not well understood, especially that this has been rarely described but is thought to be secondary to thrombosis of the small vessels supplying the myocardium. Given its rarity, there is no consensus regarding the exact management strategy but emergent plasmapheresis should be started to improve blood counts and improve clinical symptoms. Coronary angiopathy should be deferred until blood counts improve and as it may exacerbate TTP. For our patient, immediate initiation of plasmapheresis and steroids corrected her laboratory abnormalities and relieved her symptoms. Conclusion: This case represents a rare disease process that required plasmapheresis and immunosuppressives.https://scholarlycommons.henryford.com/merf2020caserpt/1112/thumbnail.jp

The Complex Management of Mechanical Prosthetic Valve Thrombosis

Mechanical prosthetic valve thrombosis (PVT) is a serious condition that is associated with various life-threatening complications. The utilization of multimodality imaging techniques is critical in identifying this etiology. Its management is complex and often requires repeat surgical valve replacements. Our report describes the case of a 48-year-old female who presented with mechanical mitral valve thrombosis in the setting of subtherapeutic anticoagulation. Due to her complex surgical history, nonsurgical therapeutic options were initially pursued for management. Through shared decision-making and after exhaustion of other alternatives, she was maintained on optimized medical therapy and was scheduled for repeat elective surgery. After compliance with medical therapy and close monitoring, she improved significantly, and her underlying pathology completely resolved, eliminating the need for surgery. This report indicates that the management of mechanical prosthetic valve thrombosis should be individualized and emphasizes the importance of involving a multidisciplinary team of medical and surgical professionals to achieve the best clinical outcomes

Quinidine hypersensitivity: a side effect of a forgotten antiarrhythmic

Quinidine is one of the oldest antiarrhythmics known. Over the years, its use has decreased along with its side effects. Our case describes a 69-year-old woman with recurrent resistant ventricular tachycardia on Quinidine and Amiodarone who presented with acute liver toxicity. Drug-induced liver toxicity was at the top of our differential diagnosis list. Taking multiple factors into consideration, a decision was made to discontinue Quinidine, the patient\u27s symptoms and lab abnormalities resolved within 1 week, yielding the diagnosis of Quinidine hypersensitivity

TCT CONNECT-245 A Meta-Analysis of Drug-Coated Balloon Versus Drug-Eluting Stent in De Novo Small Vessel Coronary Artery Disease

Background: Revascularization of small vessel coronary artery disease (SvCAD) is associated with high rate of adverse clinical outcomes. Drug-coated balloon (DCB) is an emerging alternative to drug-eluting stent (DES) in de novo SvCAD. There is limited data about the safety and outcomes of DCB in de-novo SvCAD. Methods: A meta-analysis was conducted of all studies that compared DCB and DES in de novo SvCAD. This analysis included studies with at least a 1-year follow-up from inception until April 2020. The primary outcome was all-cause mortality. Secondary outcomes included myocardial infarction, and target lesion revascularization. Following an extensive search, this is the first study to include the SCAAR (Swedish Coronary Angiography and Angioplasty Registry) report. Results: Six studies with a total of 16,591 patients were included. The median-weighted follow-up period was 2.8 years. Two of the 6 studies (BELLO [Balloon Elution and Late Loss Optimization] and BASKET-SMALL2 [Basel Stent Kosten Effektivitäts Trial Drug Eluting Balloons vs. Drug Eluting Stents in Small Vessel Interventions]) were randomized clinical trials, whereas the rest were observational studies. Heterogeneity was low to moderate across the trials (14% to 54%). In terms of the primary outcome, there was no significant difference in all-cause mortality between DCB and DES (Figure). There was also no significant difference found in the secondary outcomes of myocardial infarction and target lesion revascularization between the 2 groups. Conclusion: This meta-analysis suggests similar clinical outcomes of DCB-treated versus DES-treated de novo SvCAD. According to these results, DCB can be considered as a reasonable treatment option for SvCAD. However, further data including large randomized clinical trials are needed to confirm these results

Cholesterol induced heart valve inflammation and injury: efficacy of cholesterol lowering treatment

BACKGROUND: Heart valves often undergo a degenerative process leading to mechanical dysfunction that requires valve replacement. This process has been compared with atherosclerosis because of shared pathology and risk factors. In this study, we aimed to elucidate the role of inflammation triggered by cholesterol infiltration and cholesterol crystals formation causing mechanical and biochemical injury in heart valves. METHODS: Human and atherosclerotic rabbit heart valves were evaluated. New Zealand White male rabbits were fed an enriched cholesterol diet alone or with simvastatin and ezetimibe simultaneous or after 6 months of initiating cholesterol diet. Inflammation was measured using C-reactive protein (CRP) and RAM 11 of tissue macrophage content. Cholesterol crystal presence and content in valves was evaluated using scanning electron microscopy. RESULTS: Cholesterol diet alone induced cholesterol infiltration of valves with associated increased inflammation. Tissue cholesterol, CRP levels and RAM 11 were significantly lower in simvastatin and ezetimibe rabbit groups compared with cholesterol diet alone. However, the treatment was effective only when initiated with a cholesterol diet but not after lipid infiltration in valves. Aortic valve cholesterol content was significantly greater than all other cardiac valves. Extensive amounts of cholesterol crystals were noted in rabbit valves on cholesterol diet and in diseased human valves. CONCLUSIONS: Prevention of valve infiltration with cholesterol and reduced inflammation by simvastatin and ezetimibe was effective only when given during the initiation of high cholesterol diet but was not effective when given following infiltration of cholesterol into the valve matrix

Meta-analysis Examining the Usefulness of Angiotensin Receptor blockers for the Prevention of Aortic Root Dilation in Patients With the Marfan Syndrome

The Marfan syndrome (MFS) patients are highly predisposed to thoracic aortic aneurysm and/or dissection, with virtually every patient having evidence of aortic disease at some point during their lifetime. We conducted a meta-analysis to investigate the efficacy of angiotensin receptor blockers (ARBs) in slowing down the progression of aortic dilatation in MFS patients. PUBMED, EMBASE, and COCHRANE databases were searched for relevant articles published from inception to February 1, 2020. We included randomized clinical trials evaluating the effect of ARBs on aortic root size in patients with MFS with a follow-up period of at least 2.5 years. Seven studies were included with a total of 1,510 patients. Our analysis demonstrated a significantly smaller change in aortic root and ascending aorta dilation in the ARBs treated group when compared with placebo (mean difference 0.68; 95% confidence interval [CI] -1.31 to -0.04; p = 0.04, I(2) = 94%, and mean difference -0.13, 95% CI -0.17 to -0.09; p \u3c 0.00001, I(2) = 0%, respectively). ARBs as an add-on therapy to beta-blockers resulted in a significantly smaller change in aortic root dilation when compared with the arm without ARBs (mean difference -2.06, 95% CI -2.54 to -1.58; p \u3c 0.00001, I(2) = 91%). However, there was no statistically significant difference in the number of clinical events (aortic complications/surgery) observed in the ARBs arm when compared with placebo (Risk ratio of 1.01, 95% CI 0.74 to 1.38; p = 0.94, I(2) = 0%). In conclusion, ARBs therapy is associated with a slower progression of aortic root dilation when compared with placebo and as an addition to beta-blocker therapy