Circulation, Vol 71, 234-243, Copyright © 1985 by American Heart Association
RO Cannon 3d, DR Rosing, BJ Maron, MB Leon, RO Bonow, RM Watson and SE Epstein
To study the mechanism and hemodynamic significance of myocardial ischemia
in hypertrophic cardiomyopathy, 20 patients (nine with resting left
ventricular outflow tract obstruction greater than or equal to 30 mm Hg)
with a history of angina pectoris and angiographically normal coronary
arteries underwent a pacing study with measurement of great cardiac vein
flow, lactate and oxygen content, and left ventricular filling pressure.
Compared with 28 control subjects without hypertrophic cardiomyopathy,
their resting coronary blood flow was higher (91 +/- 27 vs 66 +/- 17
ml/min; p less than .001) and their coronary resistance was lower (1.13 +/-
0.38 vs 1.55 +/- 0.45 mm Hg/ml/min; p less than .001). Left ventricular
end-diastolic pressure (16 +/- 6 vs 11 +/- 3 mm Hg; p less than .001) and
pulmonary arterial wedge pressure (13 +/- 5 vs 7 +/- 3 mm Hg; p less than
.001) were significantly higher in patients with hypertrophic
cardiomyopathy. During pacing, coronary flow rose in both groups, although
coronary and myocardial hemodynamics differed greatly. In contrast to the
linear increase in flow in control subjects up to heart rate of 150
beats/min (66 +/- 17 to 125 +/- 28 ml/min), patients with hypertrophic
cardiomyopathy demonstrated an initial rise in flow to 133 +/- 31 ml/min at
an intermediate heart rate of 130 beats/min. At this point, 12 of 20
patients developed their typical chest pain. With continued pacing to a
heart rate of 150 beats/min, mean coronary flow fell to 114 +/- 29 ml/min
(p less than .002), with 18 of 20 patients experiencing their typical chest
pain and metabolic evidence of myocardial ischemia. This fall in coronary
flow was associated with a substantial rise in left ventricular
end-diastolic pressure (30 +/- 9 mm Hg immediately after peak pacing). In
the 14 patients whose coronary flow actually fell from intermediate to peak
pacing, the rise in left ventricular end- diastolic pressure in the same
interval was greater than that of the six patients whose flow remained
unchanged or increased (11 +/- 8 vs 2 +/- 2 mm Hg; p less than .01). In
addition, despite metabolic and hemodynamic evidence of myocardial
ischemia, the arteriovenous O2 difference actually narrowed at peak pacing.
Thus most patients with hypertrophic cardiomyopathy achieved maximum
coronary vasodilation and flow at modest increases in heart rate. Elevation
in left ventricular filling pressure, probably related to ischemia-induced
changes in ventricular compliance, was associated with a decline in
coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)
ARTICLES
Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures
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