LARGE CORONARY-ARTERY DIAMETERS ARE NOT M ATCHED TO THE MYOCARDIAL OXYGEN-DEMAND IN HYPERTENSIVE PATIENTS WITH ANGIOGRAPHICALLY NORMAL CORONARY-ARTERIES

Resting myocardial oxygen demand and corresponding coronary blood flow are main determinants of large coronary artery dimensions in humans. To examine the adaptation of epicardial coronary arteries to the incre ased myocardial oxygen deman, myocardial blood flow, in hypertensive p atients, diameters of proximal and distal left anterior descending cor onary artery (pLAD and dLAD), and proximal circumflex artery (CX) were determined in 15 untreated hypertensive patients and in 10 control su bjects by quantitative angiography. All patients had total cholesterol less than or equal to 5.40 mmol/l, LDL-cholesterol less than or equal to 3.35 mmol/l, and angiographically normal coronary arteries. Measur ements were made at base and after 2 mg intracoronary isosorbide dinit rate (ISDN) in order to obtain maximal dimensions of vessels. Coronary flow velocity was measured in distal left anterior descending coronar y artery by Doppler. Results show that despite higher rate-pressure pr oduct in hypertensive patients, the diameters of the coronary segments were similar in control subjects and in hypertensive patients at base (3.53 +/- 0.84 vs 3.76 +/- 0.48 mm for pLAD; 2.55 +/- 0.50 vs 2.49 +/ - 0.52 mm for dLAD; 2.92 +/- 0.49 vs 2.78 +/- 0.83 mm for CX, respecti vely). After intracoronary ISDN, diameters were also comparable betwee n the 2 groups (4.54 +/- 0.86 vs 4.58 +/- 0.60 mm for pLAD; 3.35 +/- 0 .58 vs 3.22 +/- 0.61 mm for dLAD; 3.47 +/- 0.56 vs 3.53 +/- 1.01 mm fo r CX, respectively). Conversely, coronary flow velocity was significan tly higher in hypertensive patients at base (10.72 +/- 2.20 vs 6.48 +/ - 2.01 cm/s; p < 0.001) and after ISDN (6.59 +/- 2.62 vs 3.72 +/- 0.87 cm/s; p < 0.001). Despite an elevated myocardial oxygen demand, large coronary artery dimensions are not increased in hypertensive patients resulting in an elevated coronary flow velocity that may increase lon gitudinal shear stress at the endothelial surface. This might be an im portant determinant in the pathogenesis of atherosclerosis in hyperten sive patients.