Links To And Excerpts From “CCTA as a Tool for Prevention in Patients with Stable Chest Pain”

In this post I link to and excerpt from CCTA as a Tool for Prevention in Patients with Stable Chest Pain [Full Text HTML]. Sep 10, 2020 | Eamon Duffy, MD; Roger S. Blumenthal, MD, FACC; Armin A. Zadeh, MD, PhD, MPH, FACC Expert Analysis. From the American College Of Cardiology.

Here are the excerpts:

Quick Takes

  • This review discusses the evidence in support of CCTA’s role for the evaluation of patients with stable chest pain, the potential function of advanced plaque assessment in this context, and the role of CCTA as a tool for CVD prevention.
  • In light of the recent PROMISE and SCOT-HEART Trials, it remains our view that the most appropriate use of CCTA in these patients is in its ability to identify and quantify atherosclerotic disease to then effectively direct the intensity of prevention strategies through lifestyle improvements and risk factor control, rather than in an effort to characterize specific plaque subtypes.

Introduction

he role of coronary computed tomography angiography (CCTA) in the evaluation of stable chest pain is an active area of research and debate. There have been multiple recent clinical trials, including SCOT-HEARTPROMISECONSERVE, and CRESCENT, that have added to the body of research supporting the role of CCTA as the first step in evaluation of these patients. This work has led the nation’s largest commercial health insurer, United Healthcare, to recently update its reimbursement policies to cover CCTA as a “first line” test to assess stable chest pain in patients with low or intermediate risk for coronary artery disease (CAD).1 Clinical guidelines in Europe have recommended CCTA first for stable chest pain for several years now, with the UK’s National Institute for Health and Care Excellence (NICE) guidelines doing so in 2016 and the European Society of Cardiology (ESC) giving it a class I recommendation more recently in 2019.2,3

The principal advantage of CCTA over stress testing is its ability to detect nonobstructive coronary atherosclerotic disease, which was associated with 77% of observed myocardial infarctions (MI) or deaths at follow up in the PROMISE trial.

This review discusses the evidence in support of CCTA’s role for the evaluation of patients with stable chest pain and the potential function of advanced plaque assessment in this context.

CCTA in Stable Chest Pain

. . . two randomized controlled trials and a large registry* consistently revealed an approximately 30% risk reduction of MI with CCTA versus stress testing. The presumed mechanism of this risk reduction is the ability of CCTA to identify CAD at an earlier stage—undetectable by stress testing—which allows initiation of preventive measures otherwise not considered.

*PROMISE, SCOT-HEART, and a Danish Registry

CCTA: A Tool for Prevention

In light of this recent work, it remains our view that the most appropriate use of CCTA in these patients is in its ability to identify and quantify atherosclerotic disease to then effectively direct the intensity of prevention strategies through lifestyle improvements and risk factor control, rather than in an effort to characterize specific plaque subtypes. Rather than a win for plaque biology, the SCOT-HEART trial, similar to the PROMISE trial, represents a win for prevention.

Combined these two large studies [PROMISE and SCOT-HEART] raise the question – how do we identify those 1% of patients that are going to have atherosclerotic events each year? It is our view that currently we cannot do so with high accuracy. The pathophysiology of acute coronary events involves many poorly understood interactions between altered atherosclerotic plaque and a thrombosis-promoting milieu, which only in the “perfect storm” scenario can combine to result in a clinically relevant ischemic event. Because of the many variables involved, it remains difficult to predict a perfect storm.4

Rather than focus on individual plaque characteristics to determine risk of future events, CCTA should be used to assess global burden of atherosclerotic disease and this should be followed by aggressive preventive care and risk factor modification.

We know that better control of blood pressure, lipids, exercise, and diet have a major impact on adverse cardiac events. However, despite clear evidence of the benefits of this secondary prevention, studies show that we significantly underperform in these efforts.17 Only half of those with hypertension have their blood pressure under control.18 A recent study found that only 58% of patients with established atherosclerotic cardiovascular disease use statins.19 Another study of patients post-MI found that one-fifth did not fill one of their cardiac medications, and half the time that medication was their antiplatelet therapy.20

The management of obstructive CAD in patients with stable chest pain is still being actively debated, with the recent ISCHEMIA trial revealing no outcome improvement with a routine invasive strategy. The results are not surprising given that coronary stenting does not address the (atherosclerotic) disease process but only mitigates its associated symptoms. PROMISE and SCOT-HEART taught us that identifying atherosclerotic disease earlier in the process leads to better outcomes. Remarkably, 77% of MIs and CV deaths in PROMISE occurred in patients with nonobstructive CAD by CCTA and 67% with normal stress test findings at baseline.22

Yet, the management of non-obstructive CAD remains highly variable, with the majority of management of non-obstructive CAD being guided by non-cardiologists.

This diagnosis of non-obstructive CAD is associated with diagnostic and therapeutic uncertainty, resulting in patients being less often treated with the appropriate secondary prevention therapies.23

The presence of non-obstructive CAD, accounting for 55% of patients in PROMISE, represents an immense opportunity for aggressive prevention. In order for this opportunity to be capitalized upon, clear guidelines must be provided to cardiologists and non-cardiologists alike that label these patients as high risk and guide treatment with aggressive preventive therapies.

Both for non-cardiologists managing non-obstructive CAD and cardiologists managing obstructive CAD, CCTA represents one of the most powerful tools in the arsenal. To best use that tool, clear guidelines are required that guide next steps for intervention and prevention.

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