Carbon monoxide poisoning and its effect on QTc prolongation.

Carbon monoxide (CO) poisoning has been associated with direct toxicity to the cardiovascular system by causing arrhythmias through prolongation of QTc. It has been reported to have arrhythmogenic potential likely due to its action on the cardiac membranes. We present a case of a 69-year-old man who presented to the emergency department for evaluation of a syncopal episode after exposure to CO. His carboxyhemoglobin level was elevated at 10.5% on admission, electrocardiogram revealed QTc interval of 622 msec. He was treated with hyperbaric oxygen and a repeat electrocardiogram 15 h after hyperbaric oxygen initiation showed improvement in QTc to 490 msec and his carboxyhemoglobin level decreased to 1.8%. There is a direct association between acute CO poisoning and QTc prolongation as reported in patient cases and evidence of it was seen by investigators who worked on rats and found that this phenomenon occurs due to the action of nitric oxide on the late Na + channels affecting repolarization. The resolution after hyperbaric oxygen could be due to decrease in the CO concentration and the absence of nitric oxide synthase activation further propagating the QT prolongation, however, further research would have to be performed to consolidate this.

Traumatic Right Coronary Artery Dissection as a Cause of Inferior Wall ST-Elevation Myocardial Infarction.

Blunt cardiac injury, causing coronary artery dissection in the absence of other forms of injury to the heart or lungs is a rare occurrence. Here we present a case of a 41-year-old male who presented with right coronary artery (RCA) dissection after blunt chest trauma. The patient initially presented with chest pain and was diagnosed with an inferior wall myocardial infarction (MI). He then developed a complete heart block and bedside echocardiogram showed right ventricular akinesis. Immediate coronary angiography showed RCA dissection, and TIMI 3 flow was established after the placement of four drug-eluting stents. Blunt trauma-induced RCA dissection is associated with high mortality which needs immediate treatment. Hence through this case report, we would like to stress the importance of having a high index of suspicion for this condition in patients with a blunt chest injury.

Flecainide toxicity in renal failure.

Flecainide, a class Ic antiarrhythmic, is used for the prevention of paroxysmal supraventricular tachycardia, paroxysmal atrial fibrillation/flutter, and sustained ventricular tachycardia. Flecainide is primarily metabolized by the liver and to a lesser extent (30%) is excreted unchanged in the kidney. We present a case of flecainide toxicity in the setting of renal impairment that was successfully treated with intravenous sodium bicarbonate.

Loperamide metabolite-induced cardiomyopathy and QTc prolongation.

Loperamide is an over-the-counter, peripherally acting, µ-opioid receptor agonist used for the treatment of diarrhea. In recent times users have found that at higher doses, loperamide crosses the blood-brain barrier and reaches central µ-receptors in the brain, leading to central opiate effects including euphoria and respiratory depression. We report a case of a 37-year-old female who attempted suicide with over 200 loperamide tablets. During her overdose, her QTc was significantly prolonged at >600 ms. Our case aims to add to the growing body of literature describing life-threatening ventricular arrhythmias associated with loperamide toxicity and further suggests that a metabolite of loperamide, desmethylloperamide, may play a role in the pathogenesis.

Are those premature ventricular complexes?!

Ventricular parasystole has been known to be a benign rhythm. We present a case of a 53-year-old man with chest pain and ventricular parasystole on electrocardiogram upon initial presentation. He was admitted and found to have normal serial cardiac enzymes and nuclear stress testing. He was discharged home with primary care follow-up. We highlight this case, as ventricular parasystole has been shown to be associated with cardiovascular disease and is a rhythm that should not be ignored. Our review of the literature shows that a thorough cardiovascular investigation should take place when this rhythm is identified.

Severe amiodarone induced pulmonary toxicity.

A known complication of Amiodarone therapy is Amiodarone induced Pulmonary Toxicity (APT). Several features of this adverse effect make it difficult to diagnosis and treat. The case of a 63-year-old male with classic radiographic and histologic findings of APT is discussed. Clinical presentation, pathophysiology, diagnostic findings, and treatment strategies are reviewed. The patient was successfully managed with pulse high dose steroid therapy.

Obesity hypertension: the regulatory role of leptin.

Leptin is a 16-kDa-peptide hormone that is primarily synthesized and secreted by adipose tissue. One of the major actions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake and elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect mechanisms, may play an important role in cardiovascular and renal regulation. While the relevance of endogenous leptin needs further clarification, it appears to function as a pressure and volume-regulating factor under conditions of health. However, in abnormal situations characterized by chronic hyperleptinemia such as obesity, it may function pathophysiologically for the development of hypertension and possibly also for direct renal, vascular, and cardiac damage.

Diagnostic and therapeutic implications of relationships between fasting, 2-hour postchallenge plasma glucose and hemoglobin a1c values.

BACKGROUND: Increased fasting plasma glucose (FPG) and 2-hour postchallenge plasma glucose (PCPG) levels with normal hemoglobin A1c (HbA1c) levels are recognized as risk factors for cardiovascular disease. We undertook this study to determine the relationships between FPG and 2-hour PCPG levels over the normal HbA1c range and to assess the need to control FPG and 2-hour PCPG levels to achieve HbA1c targets recommended by the American Diabetes Association (ADA), International Diabetes Federation (IDF), and American College of Endocrinology (ACE). METHODS: The data of all healthy individuals with HbA1c values less than 7.0% (N = 457) who underwent oral glucose tolerance tests between 1986 and 2002 for either screening as potential research volunteers (93%) or diagnostic purposes (7%) were analyzed. RESULTS: Of 404 individuals with normal HbA1c levels (<6.0%), 60% had normal glucose tolerance, 33% had impaired glucose tolerance, 1% had isolated impaired FPG, and 6% had type 2 diabetes mellitus. Of 161 individuals without normal glucose tolerance, 80% had normal FPG levels. Both FPG and 2-hour PCPG levels increased as HbA1c increased and were significantly correlated (r = 0.63, P<.001), but the 2-hour PCPG level increased at a rate 4 times greater than FPG and accounted for a greater proportion of HbA1c. People who met the IDF and ACE HbA1c targets (<6.5%) had significantly lower 2-hour PCPG levels than those who met the ADA target (<7.0%) (P =.03), whereas FPG levels were similar. CONCLUSIONS: Most individuals with HbA1c values between 6.0% and 7.0% have normal FPG levels but abnormal 2-hour PCPG levels, suggesting that an upper limit of normal for FPG at 110 mg/dL (6.11 mmol/L) is too high and that attempts to lower HbA1c in these individuals will require treatment preferentially directed at lowering postprandial glucose levels.

Serum semicarbazide-sensitive amine oxidase (SSAO) activity is an independent marker of carotid atherosclerosis.

BACKGROUND: Clinical and experimental studies suggest that increased activity of semicarbazide-sensitive amine oxidase (SSAO) and the production of cytotoxic metabolites (e.g., formaldehyde and hydrogen peroxide) may play an important role in the pathogenesis of atherosclerosis. The present study was designed to assess the relationship between the increased activity of the enzyme and the severity of atherosclerosis in diabetic and control subjects. METHODS: The study included 29 patients with type 2 diabetes mellitus and 25 control subjects. Human serum SSAO activity was determined by using 14C-benzylamine as substrate. Mean common carotid intima-media thickness (IMT), Crouse score and Bogousslawsky score was evaluated by color-coded, high-resolution duplex carotid sonography. RESULTS: Serum SSAO activity was significantly increased in patients with type 2 diabetes compared to controls. Carotid plaque score (Crouse score), total cholesterol level and age-corrected intima-media thickness showed positive correlation with enzyme activity in control subjects. In patients with diabetes, serum SSAO activity correlated with the severity of carotid stenosis (Bogousslawsky score) as well as the carotid plaque score. CONCLUSIONS: Determination of serum SSAO activity might be a candidate biochemical marker of early atherosclerosis and diabetic macrovascular complications.

Polychondritis Terminating in Eosinophilic Leukemia.

We report here on a patient presenting with Relapsing Polychondritis (RP) two years before the diagnosis of Myelodysplasia (MDS) terminating in Eosinophilic Leukemia (EoL). The evolution of RP several etiology of RP in this patient. The terminal development of EoL in our case is assumed to represent clonal evolution caused by a second mutagenic event. The existence of autoimmune skin disorders in both the patient and his offspring (vitiligo and subacute cutaneous lupus erythematosus, respectively) implies that the coexistence of MDS and RP may have been caused by a functional disturbance of the immune system.