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[Coronary microvascular dysfunction : Clinical aspects, diagnosis and therapy].

P Ong1, U Sechtem2

  • 1Abteilung für Kardiologie, Zentrum für Innere Medizin III, Robert-Bosch-Krankenhaus, Auerbachstr. 110, 70376, Stuttgart, Deutschland. Peter.Ong@rbk.de.

Herz
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PubMed
Summary

Coronary microvascular dysfunction (CMD) causes an imbalance in heart oxygen supply and demand, often presenting as angina without obstructive coronary artery disease. Further research is needed to understand its mechanisms and develop targeted treatments.

Keywords:
Angina pectorisCoronary arteriesOxygenPrognosisSecondary prophylaxis

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Area of Science:

  • Cardiology
  • Vascular Biology
  • Myocardial Pathophysiology

Background:

  • Coronary microvascular dysfunction (CMD) involves structural and functional alterations in small coronary vessels (<500 µm).
  • Mechanisms underlying CMD are diverse, overlapping, and not fully understood, with potential links to inflammation, estrogen deficiency, and genetics.
  • CMD is a common, underdiagnosed cause of angina pectoris in patients lacking obstructive epicardial coronary artery disease.

Purpose of the Study:

  • To summarize the current understanding of coronary microvascular dysfunction (CMD).
  • To highlight diagnostic approaches for CMD.
  • To discuss the clinical implications and future research directions for CMD.

Main Methods:

  • Diagnosis of CMD can be achieved through non-invasive methods like coronary computed tomography (CT) angiography combined with cardiac stress magnetic resonance imaging (MRI) or positron emission tomography (PET).
  • Invasive coronary vasomotor assessment is also a viable diagnostic option.
  • Current treatment recommendations are based on limited evidence, with European Society of Cardiology (ESC) guidelines suggesting acetylsalicylic acid (ASS), statins, beta-blockers, and/or calcium channel blockers.

Main Results:

  • Patients with CMD face an elevated annual risk of approximately 1.7% for coronary events and mortality.
  • CMD is associated with increased morbidity, leading to frequent clinical encounters and emergency hospital admissions.
  • There is a significant lack of evidence regarding the efficacy of pharmacological treatments for CMD.

Conclusions:

  • CMD represents a significant clinical challenge due to its complex pathophysiology and underdiagnosis.
  • Improved characterization of CMD mechanisms is crucial for developing effective, targeted therapeutic strategies.
  • Further clinical research is essential to advance the management and improve outcomes for patients with CMD.