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Coronary critical closing pressure during control and maximal vasodilation
ABSTRACTS
ATRIAL HYPEREMIA AND ISCHEMIA DURING ACUTE MITRAL REGURGITATION Kirit Gosalia, MD, David Sewell, MD, John Oxendine, BA, .William Neill, MD, VA Medical Center and Tufts University School of Medicine, Boston, Massachusetts Coronary blood flow (CBF) presumably is regulated by metabolic requirements for myocardial work. We determined the effects of acute increase in left atria1 (LA) pressure (P) due to mitral regurgitation (MR) on regulation of CBF to the left and right atria1 (RA) myocardium. Experiments were done in 13 open chest dogs. Graded degrees of MR (mild 7 dogs, moderate 5 dogs, severe 7 dogs) were created by severing chordae tendinae through a left ventricular apical myotomy. CBF distribution was determined by the microsphere method. CBF LAP RAP LA CBF RA mmHg rmnHg ml/min.g % total ml/min.g % total 0.47 0.27 2.2 Control 8 4 3.3 2.4* Mild MR 12* 4 0.55* 3.4 0.36* 0.75* 4.5* 0.43* 2.0* Mod. MR 20* 4 0.30" 1.9* 0.42 3.4* Sev. MR 32* 5 * Different from control, p < 0.06 Mild or moderate MR increased LAP. The LA CBF increased, and the LA received a larger percent of the total cardiac CBF. These results imply that augmented LA pressure work caused coronary vasodilation in the LA myocardium. RA CBF also increased during MR despite constant RAP, suggesting some interdependence between regulations of right and left atria1 perfusion. Severe MR with very high LAP significantly decreased LA CBF but not RA CBF. We speculate that intramyocardial compression from high LA wall tension may have impeded LA perfusion during severe MR. LA ischemia from this mechanism could contribute to atria1 arrhythmias in patients with mitral valve disease or left ventricular failure.
CORONARY CRITICAL CLOSING PRESSURE DURING CONTROL AND MAXIMAL VASODILATION Joseph A. Gascho, MD: Stanley L. Herr; Melvin L. Marcus, MD, FACC. Univ of Iowa and VA Hosns.. ” , Iowa Citv. I _ Iowa. -There is little information about critical closing pressure (CCP) in the coronary arteries. Bellamy (Circ Res 43:92, 1978) estimated by extrapolation that the diastolic CCP was 45 mmHg during control conditions, and decreased to 20 mmHg with adenosine. To further evaluate this problem, we studied pressure-flow curves in 5 chloralose anesthetized open chest dogs. We perfused the circumflex (CX) coronary artery via the femoral artery by a servo-controlled pump. This allowed us to maintain any desired pressure; flow was measured with a" electromagnetic flow meter. We studied pressure-flow curves during control conditions, and during maximal coronary vasodilation with intracoronary (IC) and intravenous (IV) adenosine. The doses of adenosine used ablated the reactive hyperemic response to coronary occlusion. CCP was determined by extrapolating the CX coronary flows at CX coronary pressures of 1929 (!&SD) to 36?4 mmHg. In this pressure range, there was an excellent linear relation between pressure and flow (mean correlation coefficient of the 15 measurements was .95+.07), and the difference between extrapolated CCP and lowest pressure measured was only 5?5 mmHg. RESULTS: HR (beats/rain) AoP (WnHg) CCP (mmHg)140?13 124+13/89+11 11+9 Control 146?12 128+15;89+8 IC Adenosine 1429 101*21* IV Adenosine *97+14/50+11* 14+9 *PC.05 vs. IC adenosine, control CONCLUSIONS: (1) During control conditions, the CCP averaged for the entire cardiac cycle is lower than previously noted. (2) IC adenosine, without systemic hemodynamic effects, or IV adenosine, with significant systemic hemodynamic effects, does not alter CCP.
CAN INTRACARDIAC VOLUME CHANGES ADEQUATELY EXPLAIN R-WAVE VARIATIONS ASSOCIATED WITH ACUIE CORONARY ISCHEMIA? Daniel David, MD, Joel Morganroth, MD, FACC, Chin C. Chen, MD, Masahito Naito, MD, Val Marcy, Eric L. Michelson, MD, Leonard S. Dreifus, MD, FACC, Lankenau Hospital, Jefferso" Medical College, Philadelphia, PA Previous human studies have attributed the increase in Rwave amplitude during coronary ischemia to a" increase in left ventricular (LV) volume (the Brody effect). To test this hypothesis, R-wave voltages (R) in leads X, Y, Z, II and V6 were compared to M-mode and cross sectional echocardiographically determined LV end diastolic volume (LVEDV) and end diastolic diameter (LVEDD) in 11 openchested dogs. The left anterior descending and circumflex coronary arteries were occluded temporarily and data collected during the hyperacute ischemic period (HIP) (1 min. after ligation (L)), during the peak ischemic period (PIP) (4-5 mins. after L), and 5 minutes after reperfusion (REP) Results are shown as percent of change from control + SE.
SELECTIVE VULNERABILITY OF THE PAPILLARY MUSCLES TO SEQUENTIAL BLOOD FLOW CHANGES INDUCED BY ISOPROTERBNOL. Franklin C. Clayton, MS; Galen M. Pieper, MS; Gordon L. Todd, PhD and Robert S. Eliot, MD, FACC, University of Nebraska Medical Center, Omaha, NE.
LVEDV LVEDD R in X R in Y R in Z R in II R in V6
HIP +27 + 4.8 +15 f 1.8 -13 + 5.1 -14 + 2.7 - 4 + 6.3 -13 + 5.1 -14 ? 2.7
PIP +44'3.6 +21 f 2.4 +13 * 6.0 +12 ? 4.2 -8f8.7 +13 ? 2.4 +17 + 6.0
+4 +2 -0.1 +0.4 -2 -3 +3
REP f 0.9 + 0.6 + 3.3 f 0.9 f 0.9 2 1.8 f 1.8
Accompanied by a progressive increase in LVEDV and LVEDD during HIP and PIP, R-wave amplitude decreases in HIP and subsequently increases in PIP and returns to control in REP. Thus, the Brody effect does not account for the initial R-wave changes during hyperacute ischemic period. Mechanisms other than the Brody effect must be considered to explain the change coronary ischemia.
in
R-wave
amplitude
during
The sequential changes in regional myocardial blood flow (MBF) following infusion of isoproterenol (ISP) were investigated with 15~ radiotracer microspheres in openchested, anesthetized dogs. They were continuously infused for one hour with a necrogenic'dose of ISP (2.5 pg/ kg/min) and MBF determined prior to and after 5, 15, 30 and 57 min of infusion. Measurements of MBF were made in four circumferential regions (anterior, lateral, posterior and septal) for each of three levels (apex, mid and base). Each tissue block was further divided into endocardial (ENDO), midmyocardial (MID) and epicardial (EPI) thirds. In general, flow increased to a plateau by 15 mln for all areaa with the left ventricular free wall END0 receiving only approximately 4 as much flow as the EPI (Control ENDO=I.20?0.05, EPI=0.91+0.04; ISP 15 min ENDO=2.67+0.16, EPI=4.18?0.27 ml/min/gm). In contrast, the anterior and posterior papillary muscle MBF did not significantly increase throughout the infusion period. There were only limited cases of heterogeneity in MBF in circumferential regions or apex to base levels. Therefore, isoproterenol stressed hearts exhibited a marked transmural gradient in MBF with a selective vulnerability of the inner layers. While END0 blood flow may be marginally adequate, the ISP-induced MBF redistribution is eve" more accentuated in the papillary muscles which can seriously affect normal cardiac function.
acute
February 1980
The American Journal of CARDIOLOGY
Volume 45
477
ATRIAL HYPEREMIA AND ISCHEMIA DURING ACUTE MITRAL REGURGITATION Kirit Gosalia, MD, David Sewell, MD, John Oxendine, BA, .William Neill, MD, VA Medical Center and Tufts University School of Medicine, Boston, Massachusetts Coronary blood flow (CBF) presumably is regulated by metabolic requirements for myocardial work. We determined the effects of acute increase in left atria1 (LA) pressure (P) due to mitral regurgitation (MR) on regulation of CBF to the left and right atria1 (RA) myocardium. Experiments were done in 13 open chest dogs. Graded degrees of MR (mild 7 dogs, moderate 5 dogs, severe 7 dogs) were created by severing chordae tendinae through a left ventricular apical myotomy. CBF distribution was determined by the microsphere method. CBF LAP RAP LA CBF RA mmHg rmnHg ml/min.g % total ml/min.g % total 0.47 0.27 2.2 Control 8 4 3.3 2.4* Mild MR 12* 4 0.55* 3.4 0.36* 0.75* 4.5* 0.43* 2.0* Mod. MR 20* 4 0.30" 1.9* 0.42 3.4* Sev. MR 32* 5 * Different from control, p < 0.06 Mild or moderate MR increased LAP. The LA CBF increased, and the LA received a larger percent of the total cardiac CBF. These results imply that augmented LA pressure work caused coronary vasodilation in the LA myocardium. RA CBF also increased during MR despite constant RAP, suggesting some interdependence between regulations of right and left atria1 perfusion. Severe MR with very high LAP significantly decreased LA CBF but not RA CBF. We speculate that intramyocardial compression from high LA wall tension may have impeded LA perfusion during severe MR. LA ischemia from this mechanism could contribute to atria1 arrhythmias in patients with mitral valve disease or left ventricular failure.
CORONARY CRITICAL CLOSING PRESSURE DURING CONTROL AND MAXIMAL VASODILATION Joseph A. Gascho, MD: Stanley L. Herr; Melvin L. Marcus, MD, FACC. Univ of Iowa and VA Hosns.. ” , Iowa Citv. I _ Iowa. -There is little information about critical closing pressure (CCP) in the coronary arteries. Bellamy (Circ Res 43:92, 1978) estimated by extrapolation that the diastolic CCP was 45 mmHg during control conditions, and decreased to 20 mmHg with adenosine. To further evaluate this problem, we studied pressure-flow curves in 5 chloralose anesthetized open chest dogs. We perfused the circumflex (CX) coronary artery via the femoral artery by a servo-controlled pump. This allowed us to maintain any desired pressure; flow was measured with a" electromagnetic flow meter. We studied pressure-flow curves during control conditions, and during maximal coronary vasodilation with intracoronary (IC) and intravenous (IV) adenosine. The doses of adenosine used ablated the reactive hyperemic response to coronary occlusion. CCP was determined by extrapolating the CX coronary flows at CX coronary pressures of 1929 (!&SD) to 36?4 mmHg. In this pressure range, there was an excellent linear relation between pressure and flow (mean correlation coefficient of the 15 measurements was .95+.07), and the difference between extrapolated CCP and lowest pressure measured was only 5?5 mmHg. RESULTS: HR (beats/rain) AoP (WnHg) CCP (mmHg)140?13 124+13/89+11 11+9 Control 146?12 128+15;89+8 IC Adenosine 1429 101*21* IV Adenosine *97+14/50+11* 14+9 *PC.05 vs. IC adenosine, control CONCLUSIONS: (1) During control conditions, the CCP averaged for the entire cardiac cycle is lower than previously noted. (2) IC adenosine, without systemic hemodynamic effects, or IV adenosine, with significant systemic hemodynamic effects, does not alter CCP.
CAN INTRACARDIAC VOLUME CHANGES ADEQUATELY EXPLAIN R-WAVE VARIATIONS ASSOCIATED WITH ACUIE CORONARY ISCHEMIA? Daniel David, MD, Joel Morganroth, MD, FACC, Chin C. Chen, MD, Masahito Naito, MD, Val Marcy, Eric L. Michelson, MD, Leonard S. Dreifus, MD, FACC, Lankenau Hospital, Jefferso" Medical College, Philadelphia, PA Previous human studies have attributed the increase in Rwave amplitude during coronary ischemia to a" increase in left ventricular (LV) volume (the Brody effect). To test this hypothesis, R-wave voltages (R) in leads X, Y, Z, II and V6 were compared to M-mode and cross sectional echocardiographically determined LV end diastolic volume (LVEDV) and end diastolic diameter (LVEDD) in 11 openchested dogs. The left anterior descending and circumflex coronary arteries were occluded temporarily and data collected during the hyperacute ischemic period (HIP) (1 min. after ligation (L)), during the peak ischemic period (PIP) (4-5 mins. after L), and 5 minutes after reperfusion (REP) Results are shown as percent of change from control + SE.
SELECTIVE VULNERABILITY OF THE PAPILLARY MUSCLES TO SEQUENTIAL BLOOD FLOW CHANGES INDUCED BY ISOPROTERBNOL. Franklin C. Clayton, MS; Galen M. Pieper, MS; Gordon L. Todd, PhD and Robert S. Eliot, MD, FACC, University of Nebraska Medical Center, Omaha, NE.
LVEDV LVEDD R in X R in Y R in Z R in II R in V6
HIP +27 + 4.8 +15 f 1.8 -13 + 5.1 -14 + 2.7 - 4 + 6.3 -13 + 5.1 -14 ? 2.7
PIP +44'3.6 +21 f 2.4 +13 * 6.0 +12 ? 4.2 -8f8.7 +13 ? 2.4 +17 + 6.0
+4 +2 -0.1 +0.4 -2 -3 +3
REP f 0.9 + 0.6 + 3.3 f 0.9 f 0.9 2 1.8 f 1.8
Accompanied by a progressive increase in LVEDV and LVEDD during HIP and PIP, R-wave amplitude decreases in HIP and subsequently increases in PIP and returns to control in REP. Thus, the Brody effect does not account for the initial R-wave changes during hyperacute ischemic period. Mechanisms other than the Brody effect must be considered to explain the change coronary ischemia.
in
R-wave
amplitude
during
The sequential changes in regional myocardial blood flow (MBF) following infusion of isoproterenol (ISP) were investigated with 15~ radiotracer microspheres in openchested, anesthetized dogs. They were continuously infused for one hour with a necrogenic'dose of ISP (2.5 pg/ kg/min) and MBF determined prior to and after 5, 15, 30 and 57 min of infusion. Measurements of MBF were made in four circumferential regions (anterior, lateral, posterior and septal) for each of three levels (apex, mid and base). Each tissue block was further divided into endocardial (ENDO), midmyocardial (MID) and epicardial (EPI) thirds. In general, flow increased to a plateau by 15 mln for all areaa with the left ventricular free wall END0 receiving only approximately 4 as much flow as the EPI (Control ENDO=I.20?0.05, EPI=0.91+0.04; ISP 15 min ENDO=2.67+0.16, EPI=4.18?0.27 ml/min/gm). In contrast, the anterior and posterior papillary muscle MBF did not significantly increase throughout the infusion period. There were only limited cases of heterogeneity in MBF in circumferential regions or apex to base levels. Therefore, isoproterenol stressed hearts exhibited a marked transmural gradient in MBF with a selective vulnerability of the inner layers. While END0 blood flow may be marginally adequate, the ISP-induced MBF redistribution is eve" more accentuated in the papillary muscles which can seriously affect normal cardiac function.
acute
February 1980
The American Journal of CARDIOLOGY
Volume 45
477