Determinants of left ventricular thrombus formation after primary percutaneous coronary intervention for anterior

LeRoy Elazar Rabbani1, Carol Waksmonski, Sohah N Iqbal

  • 1Division of Cardiology, Columbia University Medical Center, 161 Fort Washington Avenue, New York, NY 10032, USA. ler8@columbia.edu

Previous studies have reported that left ventricular (LV) thrombus is a complication in 10-56% of ST-segment elevation acute anterior wall myocardial infarctions (AWMI). Data suggest that changes in acute myocardial infarction management such as early anticoagulation, thrombolysis, and most recently, primary percutaneous coronary intervention (PCI), may decrease thrombus occurrence. Early time to reperfusion has been shown to decrease mortality and improve LV function recovery. To determine if door-to-balloon time (DTBT) affects the incidence of LV thrombus, we retrospectively analyzed data on 43 consecutive patients who underwent successful PCI of a primary acute ST-segment elevation AWMI. Transthoracic echocardiography was performed for detecting LV thrombus and measuring LV ejection fraction (EF) within 5 days on all patients (average time: 2.17 days post event). Nineteen patients underwent PCI within 2 h of arrival to the Emergency Department (Group A, average 88 min) and 24 patients underwent PCI with DTBT of more than 2 h (Group B, average 193 min). Clinically significant LV thrombus was detected in 35% of all patients. The incidence of LV thrombus formation in Group A was not significantly different from that in Group B (42.1% vs. 29.0%, respectively; P = 0.52). The risk of LV thrombus was independent of in-hospital anticoagulation and medical management, peak enzyme levels, and LVEF but did relate to age (odds ratio = 1.96, 95% CI 1.03-3.73, P = 0.04 per decade). No embolic events in hospital were observed (average hospital stay 9.2 days). We conclude that the incidence of LV thrombus remains high despite PCI. Also, we find that DTBT in patients presenting with an ST-segment elevation AWMI does not affect the incidence of LV thrombus formation. Increased age, however, does appear to increase the risk of LV thrombus development.

Related Concept Videos

Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
Pulmonary Embolism I: Introduction01:19

Pulmonary Embolism I: Introduction

A blood clot, or thrombus, is a semi-solid mass composed of fibrin, platelets, and red blood cells. When it forms within a vessel, it can obstruct blood flow, known as thrombosis. If part of the clot detaches, it becomes an embolus that can travel and block distant vessels. When this occurs in the pulmonary arteries, it causes a condition known as pulmonary embolism (PE).Origin and ImpactMost often, the embolus originates from a thrombus in the deep veins of the lower limbs, a condition called...