Recurrent and resistant angina: is the metabolic approach an appropriate answer?
1Division of Cardiology, Siena University School of Medicine, Siena, Italy. marzilli@unisi.it
Insights
Percutaneous transluminal coronary angioplasty (PTCA) offers symptomatic relief for chronic stable angina but does not reduce heart attack risk or mortality. Metabolic agents represent a new approach to managing cardiac energy metabolism in ischemic heart disease.
Area of Science:
- Cardiology
- Ischemic Heart Disease
- Interventional Cardiology
Background:
- Chronic stable angina is a primary manifestation of ischemic heart disease, affecting millions annually with significant morbidity.
- Myocardial revascularization is often pursued for symptom relief and mortality prevention in refractory angina.
- Current evidence questions the long-term benefits of revascularization for reducing myocardial infarction or mortality.
Purpose of the Study:
- To evaluate the efficacy of percutaneous transluminal coronary angioplasty (PTCA) in chronic coronary artery disease.
- To compare PTCA outcomes with medical therapy regarding symptomatic relief and hard clinical endpoints.
- To explore mechanisms contributing to persistent angina after revascularization and introduce novel therapeutic strategies.
Main Methods:
- Review of current evidence on PTCA versus medical therapy for chronic stable angina.
- Analysis of factors contributing to angina persistence post-revascularization.
- Discussion of emerging pharmacological approaches targeting cardiac energy metabolism.
Main Results:
- PTCA provides superior short-term symptomatic relief and improved exercise tolerance compared to medical therapy.
- PTCA does not significantly reduce the rates of subsequent myocardial infarction or overall mortality.
- Symptomatic benefits of PTCA diminish over time, with mechanisms like microvascular dysfunction implicated in persistent angina.
Conclusions:
- While PTCA improves angina symptoms, it does not alter the long-term prognosis regarding myocardial infarction or mortality.
- Incomplete revascularization, graft failure, disease progression, and microvascular dysfunction contribute to persistent angina.
- Metabolic agents offer a novel therapeutic avenue by targeting cardiac energy metabolism, distinct from traditional hemodynamic agents.
Abstract:
Chronic stable angina is the first manifestation of ischemic heart disease in one half of patients; in the United States, the annual incidence of angina in 213 of 1000 of the population is over 30 years of age. The morbidity associated with ischemic heart disease is considerable: each years millions of patients have an MI, or are hospitalised for unstable angina. In recent years less attention has been paid to chronic ischemic syndrome; a possible explanation is that most patients with angina, refractory to medical treatment, are referred for myocardial revascularization in order to improve symptoms and to prevent death and myocardial infarction. Unfortunately available data do not support this common belief. The current evidence allows us to conclude that percutaneous transluminal coronary angioplasty (PTCA) in chronic coronary artery disease does not reduce the rate of subsequent MI or mortality and that PTCA results in superior symptomatic relief of angina and improved exercise tolerance compared with medical therapy, but the difference narrows with time. Several mechanisms may be considered to explain the persistence of angina/ischemia after a revascularization procedure, including incomplete revascularization, graft/PTCA failure, and disease progression in native coronary arteries. Microvascular dysfunction may play a prominent role in the unexpected prevalence of angina after the removal of obstructions in the major coronary branches. A better understanding of the metabolism derangements associated with ischemia and reperfusion allowed the development of new pharmacological approaches. In contrast to classic "hemodynamic" agents, metabolic agents have no hemodynamic, inotropic or chronotropic effect and interfere with cardiac energy metabolism.
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