OBJECTIVES: The purpose of this study was to investigate whether a direct relation can be demonstrated between myocardial perfusion defects detected during dobutamine stress test (DST) by cardiovascular magnetic resonance (CMR) and impairment of coronary microvascular dilatory function in patients with cardiac syndrome X (CSX). BACKGROUND: Despite the fact that coronary microvascular dysfunction has been shown in most patients with CSX, the ischemic origin of CSX remains debated. No previous study assessed whether a strict relation exists between abnormalities in myocardial perfusion and coronary microvascular dysfunction in CSX patients. METHODS: Eighteen CSX patients (mean age 58 +/- 7 years, 7 men) and 10 healthy control subjects (mean age 54 +/- 8 years, 4 men) underwent myocardial perfusion study by gadolinium-enhanced CMR at rest and at peak DST (maximal dose 40 microg/kg/min). Coronary flow response (CFR) to adenosine (140 microg/kg/min in 90 s) in the left anterior descending (LAD) coronary artery was assessed by high-resolution transthoracic echo-Doppler and expressed as the ratio between coronary flow velocity at peak adenosine and at rest. RESULTS: At peak DST, reversible perfusion defects on CMR were found in 10 CSX patients (56%) but in none of the control subjects (p = 0.004). The CFR to adenosine in the LAD coronary artery was lower in CSX patients than in control subjects (2.03 +/- 0.63 vs. 3.29 +/- 1.0, p = 0.0004). The CSX patients with DST-induced myocardial perfusion defects in the LAD territory on CMR had a lower CFR to adenosine compared with those without perfusion defects in the LAD territory (1.69 +/- 0.5 vs. 2.31 +/- 0.6, p = 0.01). A significant correlation was found in CSX patients between CFR to adenosine and a DST perfusion defect score on CMR in the LAD territory (r = -0.45, p = 0.019). CONCLUSIONS: Our data concurrently show DST-induced myocardial perfusion defects on CMR and reduced CFR in the LAD coronary artery territory in CSX patients, thus giving strong evidence that a dysfunction of coronary microcirculation resulting in myocardial perfusion abnormalities is present in these patients.
OBJECTIVES: The purpose of this study was to investigate whether a direct relation can be demonstrated between myocardial perfusion defects detected during dobutamine stress test (DST) by cardiovascular magnetic resonance (CMR) and impairment of coronary microvascular dilatory function in patients with cardiac syndrome X (CSX). BACKGROUND: Despite the fact that coronary microvascular dysfunction has been shown in most patients with CSX, the ischemic origin of CSX remains debated. No previous study assessed whether a strict relation exists between abnormalities in myocardial perfusion and coronary microvascular dysfunction in CSXpatients. METHODS: Eighteen CSXpatients (mean age 58 +/- 7 years, 7 men) and 10 healthy control subjects (mean age 54 +/- 8 years, 4 men) underwent myocardial perfusion study by gadolinium-enhanced CMR at rest and at peak DST (maximal dose 40 microg/kg/min). Coronary flow response (CFR) to adenosine (140 microg/kg/min in 90 s) in the left anterior descending (LAD) coronary artery was assessed by high-resolution transthoracic echo-Doppler and expressed as the ratio between coronary flow velocity at peak adenosine and at rest. RESULTS: At peak DST, reversible perfusion defects on CMR were found in 10 CSXpatients (56%) but in none of the control subjects (p = 0.004). The CFR to adenosine in the LAD coronary artery was lower in CSXpatients than in control subjects (2.03 +/- 0.63 vs. 3.29 +/- 1.0, p = 0.0004). The CSXpatients with DST-induced myocardial perfusion defects in the LAD territory on CMR had a lower CFR to adenosine compared with those without perfusion defects in the LAD territory (1.69 +/- 0.5 vs. 2.31 +/- 0.6, p = 0.01). A significant correlation was found in CSXpatients between CFR to adenosine and a DST perfusion defect score on CMR in the LAD territory (r = -0.45, p = 0.019). CONCLUSIONS: Our data concurrently show DST-induced myocardial perfusion defects on CMR and reduced CFR in the LAD coronary artery territory in CSXpatients, thus giving strong evidence that a dysfunction of coronary microcirculation resulting in myocardial perfusion abnormalities is present in these patients.
Authors: Janet Wei; Puja K Mehta; B Delia Johnson; Bruce Samuels; Saibal Kar; R David Anderson; Babak Azarbal; John Petersen; Barry Sharaf; Eileen Handberg; Chrisandra Shufelt; Kamlesh Kothawade; George Sopko; Amir Lerman; Leslee Shaw; Sheryl F Kelsey; Carl J Pepine; C Noel Bairey Merz Journal: JACC Cardiovasc Interv Date: 2012-06 Impact factor: 11.195
Authors: Chrisandra L Shufelt; Louise E J Thomson; Pavel Goykhman; Megha Agarwal; Puja K Mehta; Tara Sedlak; Ning Li; Edward Gill; Bruce Samuels; Babak Azabal; Saibal Kar; Kamlesh Kothawade; Margo Minissian; Piotr Slomka; Daniel S Berman; C Noel Bairey Merz Journal: Cardiovasc Diagn Ther Date: 2013-09
Authors: Vaneet K Sandhu; Janet Wei; Louise E J Thomson; Daniel S Berman; Jay Schapira; Daniel Wallace; Michael H Weisman; C Noel Bairey Merz; Mariko L Ishimori Journal: Arthritis Care Res (Hoboken) Date: 2020-06-04 Impact factor: 4.794
Authors: I A C Vermeltfoort; P G H M Raijmakers; I I Riphagen; D A M Odekerken; A F M Kuijper; A Zwijnenburg; G J J Teule Journal: Clin Res Cardiol Date: 2010-04-21 Impact factor: 5.460