EARLY STENT THROMBOSIS

EARLY STENT THROMBOSIS- AN AUTOPSY STUDY OF LESION CHARACTERISTICS
According to a study published online ahead of print in the Journal of American college of cardiology ,patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI) face increased risk of early stent thrombosis in the presence of high thrombus burden with certain pathological traits or suboptimal stenting.

Researchers evaluated 67 stented coronary lesions from 59 patients who presented with ACS and died within 30 days of implantation (between 2004 and 2012).

Early stent thrombosis was identified in 37 lesions from 34 patients (58%), all of whom died of stent-related causes. Of 25 patients without stent thrombosis, cause of death was stent-related in 3 (distal dissection, coronary perforation, and side branch occlusion secondary to stenting). ECG readings at the time of diagnosis revealed STEMI in 16 patients and NSTEMI in 13 patients.

All 33 patients for whom pathological information on the myocardium was available had MI on histologic examination. 

Lesion Characteristics Implicated 

No differences emerged between lesions with (n = 37) or without (n = 30) stent thrombosis in terms of stent location in the coronary tree, duration of the implant, stent type (BMS vs DES or among DES types), number of stents or total stented length, or the underlying pathological findings (eg, plaque rupture, erosion, or calcified nodule).

However, in the stented segment, the maximum index thrombus thickness at the site of greatest thrombus burden was larger and necrotic core prolapse and occlusive thrombus in the side branch were more common in thrombotic lesions compared with patent lesions. Stenting in a false lumen secondary to medial dissection was numerically higher in thrombotic lesions (table 1).

Table 1. Lesion Characteristics: Thrombosis vs Patent

  Thrombosis
(n = 37 lesions)
Patent
(n = 30 lesions)
P Value
Maximum Index Thrombus Thickness, mm 0.22 0.07 0.001
Necrotic Core Prolapse 70% 43% 0.045
Side Branch Occlusion 22% 3% 0.035
False Lumen Stenting 8% 0 0.25


In nonstented segments proximal and distal to the stented segments, severe stenosis (> 75% cross-sectional narrowing), necrotic core prolapse, and medial dissection were more common in thrombotic than patent lesions, but the differences did not reach statistical significance.

 

Comparison of culprit and nonculprit sections within lesions showed that the extent of necrotic core prolapse, medial tear, and incomplete apposition was higher in sections with thrombus.

 

In particular, independent predictors of stent thrombosis on multivariate analysis were:

  • Maximum depth of strut penetration (OR 2.3; 95% CI 1.3-4.3; P = 0.006)
  • Percentage of struts with medial tear (OR 1.8; 95% CI 1.3-2.4; P = 0.001)
  • Percentage of struts with incomplete apposition (OR 1.8; 95% CI 1.4-2.4; P < 0.001)

In addition, plaque rupture was more common in arterial sections with vs without stent thrombosis (OR 2.2; 95% CI 1.5-3.2; P < 0.001).

 

 

Careful Technique, Improved Stent Designs May Help

 

The findings emphasize the potential role of intracoronary imaging in describing the underlying plaque, quantifying the lesion extent, and assessing procedural results in terms of stent apposition.

 

Improvements in stent design may help reduce stent thrombosis risk.

 

Finally, the contribution of thrombus burden to the development of stent thrombosis reinforces the importance of potent antiplatelet and anticoagulant strategies

 

 

Study Details

 

Age, sex, indication for PCI, and past medical history were similar between subjects with and without stent thrombosis.

 

 Sources:

 

1. Nakano M, Yahagi K, Otsuka F, et al. Causes of early stent thrombosis in patients with acute coronary syndrome: an ex vivohuman autopsy study. J Am Coll Cardiol. 2014;Epub ahead of print.

2. Windecker S, O’Sullivan CJ. Mitigating the risk of early stent thrombosis [editial]. J Am Coll Cardiol. 2014;Epub ahead of prin

Antiplatelet Therapy for Stable CAD in AF Patients Taking an Oral Anticoagulant

Background—The optimal long-term antithrombotic treatment of patients with coexisting atrial fibrillation and stable coronary artery disease is unresolved, and commonly, a single antiplatelet agent is added to oral anticoagulation. The study investigated the effectiveness and safety of adding antiplatelet therapy to vitamin K antagonist (VKA) in atrial fibrillation patients with stable coronary artery disease.

Methods and Results—Atrial fibrillation patients with stable coronary artery disease (defined as 12 months from an acute coronary event) between 2002 and 2011 were identified. The subsequent risk of cardiovascular events and serious bleeding events (those that required hospitalization) was examined with adjusted Cox regression models according to ongoing antithrombotic therapy. A total of 8700 patients were included (mean age, 74.2 years; 38% women). During a mean follow-up of 3.3 years, crude incidence rates were 7.2, 3.8, and 4.0 events per 100 person-years for myocardial infarction/coronary death, thromboembolism, and serious bleeding, respectively. Relative to VKA monotherapy, the risk of myocardial infarction/coronary death was similar for VKA plus aspirin (hazard ratio, 1.12 [95% confidence interval, 0.94–1.34]) and VKA plus clopidogrel (hazard ratio, 1.53 [95% confidence interval, 0.93–2.52]). The risk of thromboembolism was comparable in all regimens that included VKA, whereas the risk of bleeding increased when aspirin (hazard ratio, 1.50 [95% confidence interval, 1.23–1.82]) or clopidogrel (hazard ratio, 1.84 [95% confidence interval, 1.11–3.06]) was added to VKA.

Conclusions—In atrial fibrillation patients with stable coronary artery disease, the addition of antiplatelet therapy to VKA therapy is not associated with a reduction in risk of recurrent coronary events or thromboembolism, whereas risk of bleeding is increased significantly. The common practice of adding antiplatelet therapy to oral VKA anticoagulation in patients with atrial fibrillation and stable coronary artery disease warrants reassessment.

Circulation.2014; 129: 1577-1585