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.

Case report series of left atrial thrombus formation in patients on dabigatran therapy.

Dabigatran etexilate mesylate, a direct thrombin inhibitor, has been approved in the United States as an alternative to warfarin for the prevention of stroke and systemic thromboembolism in patients with nonvalvular atrial fibrillation. The authors report 2 cases of development of large left atrial thrombi and unfortunate occurrence of thromboembolic events in patients with chronic atrial fibrillation, despite these patients being compliant with recommended dabigatran therapy. The authors postulate that certain unique pharmacologic characteristics of the drug may be disadvantageous toward providing a therapeutic level of anticoagulation in all patients and may provide an explanation of occurrence of these thrombotic events, namely, (1) a competitive, reversible, and incomplete inhibition of only one coagulation factor (thrombin), as opposed to warfarin that leads to noncompetitive inhibition of multiple coagulation factors, (2) a short half-life (12-17 hours) and linear pharmacodynamics related to drug levels that conceivably causes an hourly variation of the level of anticoagulation, (3) a much lower incidence of supratherapeutic anticoagulation ("overshoot") with dabigatran as compared with warfarin, and (4) a reported increase in the coagulation factors that follows long-term use of dabigatran. Also, the absence of routine monitoring to test the therapeutic efficacy of the drug prevents diagnosis of cases where anticoagulation remains subtherapeutic. These factors could explain occurrence of the thrombotic and thromboembolic events in our cases.

Clinically unrecognized mitral regurgitation is prevalent in lone atrial fibrillation.

AIM: To investigate the prevalence of clinically unrecognized mitral regurgitation (MR) in lone atrial fibrillation (AF). METHODS: We studied the prevalence and severity of MR by transesophageal echocardiography (TEE) in patients with "lone" AF as compared to a matched cohort of patients in normal sinus rhythm (NSR) undergoing TEE for other indications besides recognized valvular heart disease. RESULTS: A total of 157 subjects (57 in the AF group and 100 in the NSR group) with structurally normal cardiac valves were included in the study. In the AF group, moderate MR or more was noted in 66% of the patients, mild MR in 18%, trace or no MR in 16%. In the control group, moderate MR was noted in 6% of patients, mild MR 31%, trace or no MR in 63 % of patients. Moderate MR or greater was significantly more prevalent in the AF group compared to the NSR group (66% vs 6%, P < 0.0001). CONCLUSION: Clinically unrecognized moderate MR is prevalent in "lone" AF -either as an etiologic factor leading to "lone" AF or developing after onset of AF.

Intra-graft abciximab and verapamil combined with direct stenting is a safe and effective strategy to prevent slow-flow and no-reflow phenomenon in saphenous vein graft lesions not associated with thrombus.

UNLABELLED: Slow flow and no-reflow phenomenon (SF-NR) in saphenous vein grafts (SVG) stenting is related to the occurrence of distal plaque embolization, platelet activation and microvascular vasospasm. Our article discusses few of the patents related to strategies for preventing slow-flow/no-reflow phenomenon in SVG percutaneous coronary intervention (SVG PCI). METHODS: Data from 163 consecutive patients who underwent PCI of SVG lesions without visible macro-thrombus without use of distal embolic protection device over a 10-year period were reviewed. Patients in the novel strategy group received prophylactic intra-graft administration of abciximab and verapamil followed by direct stenting (n=91). The control group (n=72) comprised of patients who had undergone conventional PCI technique before the routine availability of distal embolic protection devices, with balloon pre-dilatation of the target lesion followed by stent deployment and optional use of intragraft verapamil or intravenous abciximab. Patients with visible macro-thrombus in the vein graft were excluded from the study, since these patients underwent PCI with use of the distal embolic protection (filter). RESULTS: SF-NR (TIMI 0-1 flow) occurred more frequently in the control group compared to the novel strategy group (18% vs. 1%, P=0.0001). One patient in the control group died after developing persistent SF-NR and acute MI post-PCI. No death was reported in the novel strategy group. In the control group, 13% patients developed cardiac enzyme elevation 3 times more than normal after the PCI as compared to 1% in the novel strategy group (P < 0.05). CONCLUSIONS: In recent years several distal embolic protection devices have been granted patents for minimizing the chance of slow-flow/no-reflow phenomenon. In carefully selected subgroup of SVG lesions without visible macrothrombus, a strategy of prophylactic intra-graft administration of abciximab and verapamil, combined with direct stenting of the graft lesion without pre-dilatation, can be safely accomplished without any significant risk of slow-flow/no-reflow phenomenon. We propose a patent to this 3-step strategy of percutaneous coronary intervention of SVG lesions not associated with thrombus.

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.

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.

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.

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 obstructive coronary artery disease in patients with and without prior stroke undergoing coronary angiography for suspected coronary artery disease.

This study was conducted to investigate the prevalence and severity of obstructive coronary artery disease (CAD) in 64 men and 38 women (mean age 71+/-9 years) with previous stroke and in 102 age- and gender-matched patients with similar coronary risk factors without previous stroke who underwent coronary angiography for chest pain. Obstructive CAD was present in 100 of 102 patients (98%) with previous stroke and in 84 of 102 (82%) patients without previous stroke (p<0.001). Obstructive 3-vessel CAD was present in 56 of 102 patients (55%) with previous stroke and in 35 of 102 patients (34%) without previous stroke (p<0.005). The prevalence of 2-vessel CAD and of 1-vessel CAD was not significantly different between patients with and without previous stroke. In conclusion, patients with previous stroke have a significantly higher prevalence of obstructive CAD and of obstructive 3-vessel CAD than age- and gender-matched patients with similar coronary risk factors without previous stroke who undergo coronary angiography for chest pain.

Comparison of prevalence of unrecognized myocardial infarction and of silent myocardial ischemia detected by a treadmill exercise sestamibi stress test in patients with versus without diabetes mellitus.

We investigated, in 287 patients with diabetes (71% men; mean age 63 +/- 8 years) and 292 age- and gender-matched patients with diabetes, the prevalence of unrecognized myocardial infarction (MI) and silent myocardial ischemia (SMI) detected by a treadmill exercise sestamibi stress test. In the patients without a history of MI, MI was diagnosed by treadmill exercise sestamibi stress test in 40 of 217 patients (18%) with diabetes and 16 of 224 patients (7%) without diabetes (p <0.001). In patients with a history of angina, SMI was diagnosed in 35 of 98 patients (36%) with diabetes and 30 of 101 patients (30%) without diabetes (p = NS). In patients without a history of angina, SMI was diagnosed in 62 of 189 patients (33%) with diabetes and 35 of 191 patients (15%) without diabetes (p <0.001). In patients with 2 or 3 risk factors, SMI was diagnosed in 58 of 144 patients (40%) with diabetes and 41 of 142 patients (29%) without diabetes (p <0.005). In patients with 0 or 1 risk factor, SMI was diagnosed in 39 of 143 patients (27%) with diabetes and 24 of 150 patients (16%) without diabetes (p <0.02). In conclusion, patients with diabetes have a higher prevalence of unrecognized MI and a higher prevalence of SMI without a history of angina than patients without diabetes.

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/m in women and >134 g/m 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).

Mortality and size of abdominal aortic aneurysm at long-term follow-up of patients not treated surgically and treated with and without statins.

Of 130 patients with abdominal aortic aneurysms (AAAs) not treated surgically, 75 (58%) were treated with statins. The sizes of the AAAs were 4.6 +/- 0.6 cm at baseline and 4.5 +/- 0.6 cm at 23-month follow-up in patients treated with statins (p = NS) and 4.5 +/- 0.6 cm at baseline and 5.3 +/- 0.6 cm at 24-month follow-up in patients not treated with statins (p < 0.001). Four of 75 patients (5%) treated with statins died at 45-month follow-up, and 9 of 55 patients (16%) not treated with statins died at 44-month follow-up (p < 0.05).