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Review
. 2021 Apr;46(2):295-303.
doi: 10.1111/jcpt.13330. Epub 2021 Jan 7.

Enhanced external counterpulsation: A unique treatment for the "No-Option" refractory angina patient

Affiliations
Review

Enhanced external counterpulsation: A unique treatment for the "No-Option" refractory angina patient

Jose Caceres et al. J Clin Pharm Ther. 2021 Apr.

Abstract

What is known and objectives: Coronary artery disease (CAD) is the leading cause of death in the United States. For patients on whom guideline-driven measures have been tried, enhanced external counterpulsation (EECP) is the only truly noninvasive and safe intervention for which a reduction of angina symptoms and nitrate use, increased exercise tolerance, and improvement in myocardial ischaemia have been shown. The objective of this study was to demonstrate, by way of literature review, the efficacy of EECP as a treatment modality for the relief of refractory angina and improvement in quality of life in CAD patients.

Methods: This article reviewed the safety and efficacy of EECP in patients with refractory angina, by conducting a sweeping search and analysis of existing published literature.

Results and discussion: Critical review of a multitude of studies revealed that EECP consistently reduces angina pectoris, extends time to exercise-induced ischaemia, decreases dependency on nitroglycerine for frequent chest pain, increases maximum workload, and improves the quality of life in patients with symptomatic stable angina. The literature reviewed also indicated that EECP is well-tolerated by the vast majority of patients, with relatively few adverse events reported.

Conclusion: The present study suggests that EECP is a safe and likely best available method of treatment for patients presenting with symptomatic CAD not amenable to further revascularization.

Keywords: EECP; angina pectoris; coronary artery disease.

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Conflict of interest statement

The authors have no financial disclosures or conflicts of interest to report.

Figures

FIGURE 1
FIGURE 1
Inflation of the pneumatic cuffs, at the start of the diastole, initiates a retrograde pulse wave at the calves (A). Fifty milliseconds (ms) later, the cuffs at the thighs are inflated (B), followed by inflation of the buttocks 50 ms later (C). Simultaneous deflation begins at the end of diastole, for approximately 150 ms, which facilitates systolic unloading (D)
FIGURE 2
FIGURE 2
The first three cardiac cycles depict a normal finger plethysmographic recording in the absence of counterpulsation (control). In the presence of counterpulsation (EECP), as seen in the last three cycles, there is a decrease in systolic pressure—“systolic unloading” (first hump)—and a marked rise in peak arterial diastolic pressure—“diastolic augmentation” (second hump)—resulting in an increase of coronary blood flow and coronary perfusion pressure. EECP, Enhanced External Counterpulsation
FIGURE 3
FIGURE 3
Central and peripheral mechanisms of EECP. VEGF‐Vascular endothelial growth factor; BFGF‐Basic fibroblast growth factor; HGF‐Hepatocyte growth factor; TNF‐a‐Tumour necrosis factor‐alpha; MCP‐1‐Monocyte chemoattractant protein‐1; VCAM‐1‐Vascular cell adhesion molecule‐1; BNP‐Brain natriuretic peptide; ANP‐Atrial natriuretic peptide; ACE‐Angiotensin‐converting enzyme; ANG II‐Angiotensin II; EECP, Enhanced External Counterpulsation

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