Rasham Sandhu

Relation of Cardiac Troponin I Levels With In-Hospital Mortality in Patients With Ischemic Stroke, Intracerebral Hemorrhage, and Subarachnoid Hemorrhage

Troponin I levels were drawn within 24 hours of stroke in 161 of 175 patients (92%) with ischemic stroke, 94 of 107 patients (88%) with intracerebral hemorrhage, and 96 of 96 patients (100%) with subarachnoid hemorrhage. A troponin level >0.4 ng/ml was considered increased. In patients with ischemic stroke, in-hospital mortality occurred in 15 of 23 patients (65%) with increased troponin I compared with 6 of 138 patients (4%) with normal troponin I (p <0.001). In patients with intracerebral hemorrhage, in-hospital mortality occurred in 9 of 14 patients (64%) with increased troponin I compared with 22 of 80 patients (28%) with normal troponin I (p <0.005). In patients with subarachnoid hemorrhage, in-hospital mortality occurred in 8 of 20 patients (40%) with increased troponin I compared with 8 of 76 patients (11%) with normal troponin I (p <0.005). In conclusion, patients with ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage with elevated troponin I levels have increased in-hospital mortality.

Warfarin use and the risk of valvular calcification.

Summary.  Background: Warfarin affects the synthesis and function of the matrix Gla‐protein, a vitamin K‐dependent protein, which is a potent inhibitor of tissue calcification. Objectives: To investigate the incidence of mitral valve calcium (MVC), mitral annular calcium (MAC) and aortic valve calcium (AVC) in patients with non‐valvular atrial fibrillation (AF) treated with warfarin vs. no warfarin. Patients and methods: Of 1155 patients, mean age 74 years, with AF, 725 (63%) were treated with warfarin and 430 (37%) without warfarin. The incidence of MVC, MAC and AVC was investigated in these 1155 patients with two‐dimensional echocardiograms. Unadjusted logistic regression analysis was conducted to examine the association between the use of warfarin and the incidence of MVC, MAC or AVC. Logistic regression analyses were also conducted to investigate whether the relationship stands after adjustment for confounding risk factors such as age, sex, race, ejection fraction, smoking, hypertension, diabetes, dyslipidemia, coronary artery disease (CAD), glomerular filtration rate, calcium, phosphorus, calcium‐phosphorus product, alkaline phosphatase, use of aspirin, beta blockers, angiotensin‐converting enzyme inhibitors or angiotensin receptor blockers, and statins. Results: There was a significant association between the use of warfarin and the risk of calcification [unadjusted odds ratio = 1.71, 95% CI = (1.34–2.18)]. The association still stands after adjustment for confounding risk factors. MVC, MAC or AVC was present in 473 of 725 patients (65%) on warfarin vs. 225 of 430 patients (52%) not on warfarin (P < 0.0001). Whether this is a causal relationship remains unknown. Conclusions: Use of warfarin in patients with AF is associated with an increased prevalence of MVC, MAC or AVC.

Prevalence of left ventricular hypertrophy in persons with and without obstructive sleep apnea.

We investigated the prevalence of left ventricular hypertrophy (LVH) in persons with and without obstructive sleep apnea (OSA). Fifty-three persons had a nocturnal polysomnogram to diagnose OSA and 2-dimensional echocardiograms to measure left ventricular mass. OSA was considered mild if the respiratory disturbance index (RDI) was 5 to 15, moderate if the RDI was 15 to 30, and severe if the RDI was >30. LVH was diagnosed if the left ventricular mass index was >110 g/m2 in women and >134 g/m2 in men. LVH was present in 21 of 27 persons (78%) with moderate or severe OSA, in 6 of 13 persons (46%) with mild OSA, and in 3 of 13 persons (23%) with no OSA (P < 0.001 comparing moderate or severe OSA with no OSA and P < 0.05 comparing moderate or severe OSA with mild OSA). OSA was a significant independent predictor of LVH after controlling the confounding effects of hypertension with an odds ratio of 3.579 (95% confidence interval, 1.589–8.058).

Brugada electrocardiographic pattern induced by amitriptyline overdose.

Tricyclic antidepressants (TCAs) remain a common cause of fatal drug poisoning as a result of their cardiovascular toxicity manifested by electrocardiographic abnormalities, arrhythmias, and hypotension. The principal mechanism of toxicity is cardiac sodium channel blockade. Brugada electrocardiographic pattern (BEP) has also been described in TCA overdose. Currently, very little is known about the relationship between the Brugada syndrome and TCAs. We report the case of a patient who presented with BEP after intake of a high dose of amitriptyline. The patient was treated with continuous sodium bicarbonate infusion leading to resolution of BEP.

Extensive fatal intracoronary thrombosis during percutaneous coronary intervention with bivalirudin.

The authors describe 2 cases of extensive intracoronary thrombus formation leading to acute closure of the left main where bivalirudin (Angiomax) was used as the anticoagulant during percutaneous coronary intervention leading to mortality. Both cases had similarity in the cascade of complications of coronary dissection leading to slow flow and prolonged procedure time with compromise of antegrade flow in the coronary artery and a final catastrophic development of extensive intracoronary thrombosis extending into the left main and nonintervened vessel (left anterior descending or circumflex) followed by ventricular fibrillation and death. Bivalirudin has reversible anticoagulant pharmacodynamics because the bivalirudin molecule is cleaved by the thrombin molecule. In situations when the antegrade flow is compromised, delivery of fresh circulating bivalirudin to replenish the catalysis of bivalirudin by thrombin is diminished, allowing thrombin activity to regenerate, thereby creating a prothrombotic milieu in these coronary segments. This can lead to extensive intracoronary thrombus formation in situations of slow flow precipitated by coronary dissection and prolonged dwell time with intracoronary hardware (wires, balloons, and stents). Interventionalists should be aware of the potential risk of this fatal complication and should be proactive in recognizing the scenarios where this is likely to occur. In such anticipated circumstances, the interventionalist may judiciously switch the anticoagulant to heparin and/or use additional glycoprotein IIb/IIIa inhibitor because freshly formed intracoronary thrombus is susceptible to lysis by glycoprotein IIb/IIIa inhibitors.

Pseudoaneurysm with thrombus and left ventricular inflow obstruction after left circumflex stenting.

A 61-year-old woman had stenting of the left circumflex coronary artery. She had a repeat coronary angiogram the day after stenting because of hypotension and orthopnea. The left circumflex stent was patent. A transesophageal echocardiogram showed a 2.5 cm x 3.0-cm mass in the atrioventricular groove compressing the left atrium. A pseudoaneurysm with thrombus and left ventricular inflow obstruction was diagnosed. The patient was observed for 48 hours to allow the pseudoaneurysm to seal and coagulate. She then had surgical evacuation of the thrombus, which had caused her hypotension and orthopnea by compression of the left atrium.

Prevalence of in-hospital complications in 500 patients undergoing percutaneous coronary intervention treated with heparin 5000 IU administered systemically versus 500 age-matched and sex-matched patients treated with heparin 70 IU/kg administered systemically.

We investigated the prevalence of in-hospital complications in 500 patients undergoing percutaneous coronary intervention (PCI) treated with heparin 5000 IU administered systemically (group 1) at the time of PCI versus in 500 age-matched and sex-matched patients undergoing PCI treated with heparin 70 IU/kg administered systemically (group 2) at the time of PCI. There was no significant difference in baseline characteristics, indications for PCI, cardiovascular drug therapy at the time of PCI, prevalence of 1-vessel, 2-vessel, and 3-vessel obstructive coronary artery disease, and in-hospital complications between the 2 groups. In-hospital death occurred in 0.2% of group 1 patients versus 0.8% of group 2 patients. Non-ST-segment elevation myocardial infarction occurred in 0.2% of group 1 patients versus 0.4% of group 2 patients. Stroke occurred in 0.2% of group 1 patients versus 0.2% of group 2 patients. Stent thrombosis occurred in 0.2% of group 1 patients versus 0.8% of group 2 patients. Occlusion of a side branch occurred in 0.2% of group 1 patients versus 0.4% of group 2 patients. A hematoma needing intervention occurred in 0.2% of group 1 patients versus 0.2% of group 2 patients. Regression analysis showed that none of the differences between the 2 groups were significant. The sample size was adequate to conclude that a fixed low dose of heparin 5000 IU administered systemically at the time of PCI is noninferior to standard therapy with heparin.