PMID- 20560003 OWN - NLM STAT- MEDLINE DCOM- 20101102 LR - 20211020 IS - 1937-5395 (Electronic) IS - 1937-5387 (Linking) VI - 2 IP - 4 DP - 2009 Dec TI - Microvascular dysfunction, myocardial ischemia, and progression to heart failure in patients with hypertrophic cardiomyopathy. PG - 452-61 LID - 10.1007/s12265-009-9142-5 [doi] AB - Microvascular dysfunction can be demonstrated in most patients with hypertrophic cardiomyopathy (HCM), both in the hypertrophied and nonhypertrophied myocardial walls, mostly due to intimal and medial hyperplasia of the intramural coronary arteries and subsequent lumen reduction. As a consequence, regional myocardial ischemia may be triggered by exercise, increased heart rate, or arrhythmias, in areas which are unable to increase myocardial blood flow. In patients with HCM, microvascular dysfunction leading to severe myocardial hypoperfusion during maximal hyperemia represents a strong predictor of unfavorable outcome, left ventricular remodeling with progressive wall thinning, left ventricular dysfunction, and heart failure. Accurate quantitative assessment of microvascular dysfunction and myocardial ischemia is not easily feasible in clinical practice. Although signs of inducible myocardial ischemia may be detected by electrocardiogram, echocardiography, or myocardial scintigraphy, the vasodilator response to dipyridamole by positron emission tomography is considered the method of choice for the assessment of maximal regional and global flow. Cardiac magnetic resonance provides further information, by late gadolinium enhancement (LGE), which may show areas where replacement fibrosis has occurred following microvascular ischemia and focal necrosis. LGE areas colocalize with severe regional microvascular dysfunction, are associated with increased prevalence of ventricular arrhythmias, and show more extensive distribution in the late stages of the disease, when heart failure is the dominant feature. The present review aims to provide a concise overview of the available evidence of microvascular dysfunction and ischemia eventually leading to disease progression and heart failure in HCM patients. FAU - Cecchi, Franco AU - Cecchi F AD - Regional Referral Center for Myocardial Diseases, Department of Cardiology, Azienda Ospedaliera Universitaria Careggi, Florence, Italy. cecchif@aou-careggi.toscana.it FAU - Sgalambro, Aurelio AU - Sgalambro A FAU - Baldi, Massimo AU - Baldi M FAU - Sotgia, Barbara AU - Sotgia B FAU - Antoniucci, Davide AU - Antoniucci D FAU - Camici, Paolo G AU - Camici PG FAU - Sciagra, Roberto AU - Sciagra R FAU - Olivotto, Iacopo AU - Olivotto I LA - eng PT - Journal Article PT - Review DEP - 20091103 PL - United States TA - J Cardiovasc Transl Res JT - Journal of cardiovascular translational research JID - 101468585 SB - IM MH - Arrhythmias, Cardiac/etiology/physiopathology MH - Cardiomyopathy, Hypertrophic/*complications/physiopathology MH - Coronary Circulation MH - Coronary Vessels/*physiopathology MH - Disease Progression MH - Exercise MH - Heart Failure/*etiology/physiopathology MH - Humans MH - Microcirculation MH - Microvessels/*physiopathology MH - Myocardial Ischemia/*etiology/physiopathology MH - Risk Factors MH - Ventricular Outflow Obstruction/etiology/physiopathology EDAT- 2010/06/19 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/06/19 06:00 PHST- 2009/09/14 00:00 [received] PHST- 2009/10/05 00:00 [accepted] PHST- 2010/06/19 06:00 [entrez] PHST- 2010/06/19 06:00 [pubmed] PHST- 2010/11/03 06:00 [medline] AID - 10.1007/s12265-009-9142-5 [doi] PST - ppublish SO - J Cardiovasc Transl Res. 2009 Dec;2(4):452-61. doi: 10.1007/s12265-009-9142-5. Epub 2009 Nov 3.