Decitabine induced transient cardiomyopathy: a case report.

CASE REPORT: A 75-yr-old gentleman, with a past medical history of diabetes mellitus and Acute Myeloid Leukemia presented to our emergency department with a chief complaint of exertional dyspnea and chest pain. A week prior to this visit, he had recieved a cycle of decitabine chemotherapy at 20 mg/metered square for ten days. This was his second cycle of decitabine. His out patient medications included megesterol, omeprazole, morphine sulfate and insulin glargine. The patient was admitted to the Coronary Care Unit for Acute Coronary Syndrome. His cardiac enzymes were elevated (peak troponin 30 ng/mL, CKMB 67.4 ng/mL). His 12 lead EKG revealed sinus tachycardia with a ventricular rate of 113, but without acute ST-T wave changes. The BNP was 259 pg/mL. A 2D echo revealed moderate diffuse hypokinesis with an EF of 35%. He subsequently underwent a left heart catheterization, which showed non-obstructive CAD. In our patient, the elevated troponins (peak troponin 30 ng/mL) and BNP were seen concomitant with the onset of cardiogenic shock. Two months ago, his 2 D echocardiogram revealed an ejection fraction of about 55%-65% with slightly increased left ventricular (LV) wall thickness. DISCUSSION: The most common adverse effects of decitabine include cytopenia, nausea, pain and erythema/nodules at the injection site. To date, there has been only one reported case of a hypomethylating agent inducing acute myocarditis. We a present a case of reversible, non-ischemic cardiomyopathy secondary to decitabine chemotherapy, which resolved after the drug was discontinued. Trials involving decitabine for the treatment of MDS reported no myocarditis. In our case, the diagnosis of transient cardiomyopathy was highly probable since the patient's troponins and echocardiogram returned to baseline after discontinuation of treatment. Also, the patient never had any further chest pain at his 6 month follow up. In this case, we believe that the elevated Troponin I levels, along with a cardiac catheterization revealing patent coronary vessels, favor our hypothesis that our patient suffered from acute myocarditis as a result of direct toxicity from decitabine chemotherapy. We doubt that there was an underlying infectious etiology, since the patient had three negative blood cultures, two negative urine cultures and a negative viral serology. Our case demonstrates that chest pains in a patient treated with hypomethylating agents should be further explored in order to rule out acute myocarditis.

Serum lipoprotein levels in takotsubo cardiomyopathy vs. myocardial infarction.

BACKGROUND: In the setting of myocardial infarction (MI) or acute coronary syndrome (ACS), current guidelines recommend early and aggressive lipid lowering therapy with statins, irrespective of the baseline lipoprotein levels. Takotsubo cardiomyopathy (TCM) patients have a clinical presentation similar to myocardial infarction and thus receive early and aggressive statin therapy during their initial hospitalization. However, the pathology of TCM is not atherosclerotic coronary artery disease and hence we assumed the lipid profiles in TCM would be healthier than coronary artery disease patients. METHODS: In this retrospective study, we assessed fasting serum lipoprotein levels of ten TCM patients and compared them with forty, age and sex-matched myocardial infarction (MI) patients. RESULTS: Comparing serum lipoprotein levels of TCM with MI group, there was no significant difference in mean total cholesterol between the two groups (174.5 mg/dL vs. 197.6 mg/dL, p = 0.12). However, in the TCM group, mean HDL-C was significantly higher (66.87 mg/dL vs. 36.5 mg/dL, p = 0.008), the mean LDL-C was significantly lower (89.7 mg/dL vs. 128.9 mg/dL, p = 0.0002), and mean triglycerides was also significantly lower (65.2 mg/dL vs. 166.8 mg/dL, p < 0.0001). CONCLUSIONS: In this study, TCM patients in comparison to MI patients had significantly higher levels of HDL-C, lower levels of LDL-C levels and triglycerides. The lipid profiles in TCM were consistent with the underlying pathology of non-atherosclerotic, non-obstructive coronary artery disease. As lipoproteins in most TCM patients were within the optimal range, we recommend an individual assessment of lipid profiles along with their coronary heart disease risk factors for considering long term lipid-lowering therapy. A finding of hyperalphalipoproteinemia or hypotriglyceridemia in 40% of TCM patients is novel but this association needs to be confirmed in future studies with larger sample sizes. These findings may provide clues in understanding the pathogenesis of takotsubo cardiomyopathy.

Complete recovery of ischemic cardiomyopathy from thrombotic thrombocytopenic purpura.

A 50 year old male HIV patient on antiretroviral therapy was admitted for chest pain. Upon admission, the patient was found to have elevated cardiac enzymes, acute thrombocytopenia, hemolytic anemia, acute pancreatitis and acute renal failure. The patient was diagnosed with thrombotic thrombocytopenic purpura/haemolytic uremic syndrome and emergency plasma exchange therapy was initiated along with aspirin, beta-blockers, steroids, and antiretroviral therapy. Patient responded well and demonstrated complete resolution of ischemic cardiomyopathy with left ventricular ejection fraction improving from 35% to 55% by the time of discharge. Essentially, prompt diagnosis and treatment can reverse cardiac damage induced by thrombotic thrombocytopenic purpura.

Ryanodine calcium channel: a novel channelopathy for seizures.

INTRODUCTION: Catecholamine-induced polymorphic ventricular tachycardia (CPVT) is one of the most severe inherited arrhythmogenic disorders, where patients clinically present with syncope or seizures. CASE: An 18-year-old white male with a history of mild developmental delay and CPVT, was brought to the ED after an episode of unresponsiveness for several minutes. The EMS documented a rhythm strip showing sinus tachycardia. The patient was awake and alert with no clinical evidence of any focal neurologic deficits, but unable to recall the event. Initial blood works including cardiac enzymes were normal. EKG showed sinus rhythm at 86 bpm, along with bigeminy and couplets of bidirectional QRS morphology with a QT interval of 0.3 seconds. Imaging studies including computed tomography scans of head, magnetic resonance imaging of brain, and 2D cardiac echo were normal. A routine EEG revealed abnormal bursts of spike and aftergoing slow wave complexes, highly suggestive of a potential for seizure activity. A 24-hour video EEG-EKG confirmed abnormal brain activity in the presence of normal sinus rhythm. A recent experimental study showed that knock in models of mice mutated with leaky calcium channels in the heart and brain exhibited seizures independent of arrhythmias. CONCLUSIONS: Our patient is probably the clinical paradigm of this study. This episode of unresponsiveness, most probably a complex partial seizure, may have been caused by the same mutations known to precipitate CPVT.

Proximal atherosclerotic lesion as a cause of very late stent thrombosis.

Very late stent thrombosis is defined as in-stent thrombosis occurring after 1 year of an intra-coronary artery stent placement. Drug eluting stents have lately been criticized for increased reports of very late stent thrombosis. The exact cause of these very late stent thromboses is not clearly understood. Virchow's triad describes the three main factors of thrombus formation to be stasis of blood flow, endothelial injury and hypercoagulability. Based on Virchow's triad, we propose the cause of very late stent thrombosis to be formation of a de novo atherosclerotic lesion in the proximal segment of a stented artery. The de novo atherosclerotic lesion narrows the vessel lumen and causes stasis of blood flow in the distal stent. The de novo lesion can also cause myocardial ischemia creating a prothrombotic environment in the stented region. Stasis of blood flow and prothrombotic environment in the stented region can lead to the formation of very late stent thrombosis. Since atherosclerosis is a dynamic aging process in humans, we propose de novo proximal lesions in the coronary arteries can predispose to very late stent thrombosis.

In-stent thrombosis after 68 months of implantation inspite of continuous dual antiplatelet therapy: a case report.

Lately, there has been an increased incidence of late stent thrombosis; especially following Drug eluting stent (DES) implantation. Several factors are associated with an increased risk of stent thrombosis, including the procedure itself, patient and lesion characteristics, stent design, and premature cessation of anti-platelet drugs. We present a case of late stent thrombosis (LST) following DES implantation after a period of 68 months, making it the longest reported case of LST reported in the literature, despite the use of dual anti-platelet therapy.

Tamponade following breast augmentation.

Breast augmentation is one of most commonly performed cosmetic surgical procedures. Pneumothorax has been reported as a rare complication of breast augmentation but the incidence is not known. Our patient presented with dyspnea on exertion about 6 days following breast augmentation. She was found to have cardiac tamponade and pneumothorax. We present a case of cardiac tamponade following breast augmentation, a previously unreported complication.