Effect of exercise on coronary pressure-flow relationship in hypertrophied left ventricle

1995 ◽  
Vol 269 (1) ◽  
pp. H271-H281 ◽  
Author(s):  
D. J. Duncker ◽  
J. Zhang ◽  
T. J. Pavek ◽  
M. J. Crampton ◽  
R. J. Bache
Keyword(s):  
Coronary Artery ◽  
Myocardial Perfusion ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Back Pressure ◽  
Pressure Flow ◽  
Pronounced Increase ◽  
Coronary Pressure

Left ventricular (LV) hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during exercise. The present study was performed to determine whether exercise causes alterations in minimum coronary resistance or effective back pressure [coronary pressure at zero flow (Pzf)] that limit maximum myocardial perfusion in the hypertrophied heart. Ascending aortic banding in 7 dogs increased the LV weight-to-body weight ratio to 7.7 +/- 0.3 g/kg compared with 4.6 +/- 0.2 g/kg in 11 normal dogs (P < 0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. Under resting conditions, the slope of the pressure-flow relationship (conductance) was significantly lower in the LVH animals than in the normal dogs (7.2 +/- 0.8 vs. 11.9 +/- 0.8 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01); the slope correlated with the degree of hypertrophy r = 0.74; P < 0.001). The Pzf measured during total coronary artery occlusion (Pzf,measured) was significantly elevated in LVH compared with normal dogs (25.6 +/- 2.2 vs. 13.0 +/- 1.2 mmHg; P < 0.01); Pzf,measured was positively correlated (r = 0.78, P < 0.0005) with LV end-diastolic pressure measured during total coronary artery occlusion (9.0 +/- 1.1 mmHg in normal dogs and 22.2 +/- 3.2 mmHg in LVH dogs; P < 0.01). Graded treadmill exercise to maximum heart rates of 210 +/- 9 and 201 +/- 8 beats/min in normal and LVH animals, respectively, caused similar decreases in the slope of the pressure-flow relationship in LVH (from 7.7 +/- 0.9 to 6.1 +/- 0.8 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01) and normal dogs (from 11.9 +/- 0.8 to 10.0 +/- 0.7 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01). However, exercise-induced increases in Pzf,measured were significantly greater in the LVH animals (from 25.6 +/- 2.2 to 40.8 +/- 2.1 mmHg; P < 0.01) than in normal animals (from 13.0 +/- 1.2 to 24 +/- 2.1 mmHg; P < 0.01) (P < 0.01 LVH vs. normal). The greater increase in Pzf paralleled a more pronounced increase in LV end-diastolic pressure in the LVH dogs from 22.2 +/- 3.2 to 39.1 +/- 2.7 mmHg) than in normal dogs from 9.0 +/- 1.1 to 14.2 +/- 2.0 mmHg). The results suggest that exaggerated increases in filling pressure during exercise in the hypertrophied left ventricles contributed to impairment of myocardial perfusion during exercise by augmenting the back pressure, which opposes coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Abstract 3341: Human Coronary Collaterals Inversely Correlate with Indices of Ischemic Left Ventricular Diastolic Dysfunction during Coronary Balloon Occlusion.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stephen P Hoole ◽  
Paul A White ◽  
Patrick M Heck ◽  
Michael O’Sullivan ◽  
Sarah C Clarke ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Flow Index ◽  
Collateral Flow ◽  
Coronary Collaterals

Background: Coronary collaterals are thought to reduce myocardial ischemia during coronary artery occlusion. Coronary collaterals, defined angiographically, reduce end diastolic LV dilatation during coronary occlusion. However, counter to a role in reducing ischemia, they appear to be associated with an increase in LV end diastolic pressure. These changes may be explained if coronary collaterals act as an external LV scaffold. We aimed to re-evaluate this relationship by simultaneously measuring coronary collaterals and LV contractility quantitatively. Methods: Ten patients with normal LV function and single vessel coronary disease awaiting PCI were recruited. Collateral flow index, derived by pressure-wire measurement (CFI p = [P distal (occluded) − P venous ] / [P aorta − P venous ]) and change in LV end-diastolic pressure (LVEDP), volume (LVEDV) and Tau, measured by an LV cavity conductance catheter, were recorded simultaneously after 1 minute coronary balloon occlusion. A mean of 5 cardiac cycles was analyzed. Measurements were repeated after a recovery period of 30 minutes. Results: Percentage change in LVEDP and Tau inversely correlated with CFI p (ΔLVEDP vs. CFI p : y = −216.6x +63.4, r = 0.57, p=0.01; ΔTau vs. CFI p : y = −64.1x + 27.8, r = 0.47, p<0.05) (Figure ). There was also an inverse relationship between ΔLVEDV vs. CFI p (y = −8.4x + 1.5, r = 0.35, p = 0.15). Conclusion: Coronary collaterals inversely correlate with LV end diastolic stiffness and dilatation after 1 minute of coronary artery occlusion. This reflects a role in reducing ischemic LV diastolic dysfunction, by providing an alternative blood supply to the LV myocardium, rather than acting as an LV scaffold.

Innate protection of baboon myocardium: effects of coronary artery occlusion and reperfusion

1996 ◽  
Vol 270 (5) ◽  
pp. H1812-H1818 ◽  
Author(s):  
Y. T. Shen ◽  
J. T. Fallon ◽  
M. Iwase ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Infarct Size ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Area At Risk ◽  
Protective Mechanisms ◽  
Reperfusion Period

To determine whether the extent of myocardial infarction differs in conscious baboons and pigs, both devoid of performed collaterals, the effects of 40 and 90 min of coronary artery (CA) occlusion (O) both followed by 4-7 days of CA reperfusion (R) were examined in both species. CAO reduced subendocardial and subepicardial blood flows similarly, almost to zero, in baboons and pigs for the entire CAO period. At 24 h of CAR, subendocardial blood flow had almost returned to pre-CAO control levels in baboons but remained significantly depressed in pigs. The major difference in hemodynamics during CAO and CAR was in left ventricular end-diastolic pressure, which rose by 6 +/- 1 mmHg in pigs over the initial 24-h reperfusion period but did not change significantly in baboons. These data on recovery of subendocardial blood flow and left ventricular end-diastolic pressure suggest larger infarcts in pigs than in baboons. Indeed, infarct size expressed as a function of area at risk (IF/AAR) was significantly greater (P <0.05) in pigs (53 +/- 4.9%) than in baboons (17 +/- 2.9%) with 90 min of CAO and 4-7 days of CAR. With 40 min of CAO and 4-7 days of CAR, IF/AAR was 46 +/- 3.6% in pigs, whereas in baboons the IF/AAR was minimal, i.e., 2 +/- 0.6%. Thus pigs and baboons were characterized by minimal coronary collateral circulation, but infarct size was significantly less in conscious baboons than in conscious pigs. Potentially, these differences could be explained, in part, by natural protective mechanisms and/or less reperfusion injury in primates. These results in primates may also help explain the salutary effects of CAR in patients at intervals longer than have been demonstrated to be beneficial in other experimental animals.

Effect of activation sequence on MVO2 before and after coronary ligation

1978 ◽  
Vol 234 (3) ◽  
pp. H260-H265
Author(s):  
A. C. Kralios ◽  
T. J. Tsagaris
Keyword(s):  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Systemic Arterial Pressure ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Work Index ◽  
Before And After ◽  
Ventricular Activation ◽  
Ectopic Activation ◽  
Activation Sequence

In pentobarbital-anesthetized, open-chest dogs with fixed heart rate, cardiac output, and systemic arterial pressure, ectopic ventricular activation originating from apical as compared to basilar regions of either ventricle was associated with small (3--5%) but significantly (P less than 0.005) lower myocardial O2 consumption (MVO2) and thus higher left ventricular (LV) efficiency without change in LV end-diastolic pressure (LVEDP), work index (LVWI), and LV dP/dt. Data obtained during epicardial and corresponding endocardial activation did not differ. During normal ventricular activation, MVO2 remained unchanged but LVEDP was significantly (P less than 0.005) lower, thus yielding higher LVWI and efficiency. MVO2 differences among ectopic sites were abolished after coronary artery occlusion, whereas data obtained during endocardial and epicardial on normal and ectopic activation were not affected. Thus, normal activation resulting in lower LVEDP is most efficient; apical ventricular activation is less efficient at the same MVO2P basilar is the least efficient, because both MVO2 and LVEDP are higher. Ventricular activation sequence changes do not constitute a substantial determinant of MVO2.

Long-Term Effects of Growth Hormone on Infarct Size and Left Ventricular Function in Sheep With Coronary Artery Occlusion

2010 ◽  
Vol 55 (3) ◽  
pp. 255-261
Author(s):  
Fernanda D Olea ◽  
Andrea De Lorenzi ◽  
Claudia Cortés ◽  
Patricia Cabeza Meckert ◽  
Oscar Cendoya ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Coronary Artery ◽  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Long Term Effects
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