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Failure of intracoronary nitroglycerin to alleviate pacing-induced angina
ABSTRACTS
of the Wenckebach cycle is blocked retrograde is due to a collision of the reentrant and the retrograde wavefronts. A similar mechanism may explain antegrade Wenckebach. Failure of lntracoronary Pacing-Induced Angina
Nitroglycerin
to Alleviate
WILLIAM GANZ, MD, FACC*; HAROLD S. MARCUS, MD, Los Angeles, California
To assess the role of the direct effects of nitroglycerin (NTG) on the coronary circulation in the relief of angina, NTG was injected after induction of angina by pacing into the left (LCA) or right coronary artery (RCA) ; the doses were too small to cause a significant decrease in arterial blood pressure but in normal subjects were sufficient to augment coronary sinus blood flow (CSBF) by 50 to 100% for 30 to 60 seconds. After insertion of the angiographic catheter into the LCA, angina was induced by pacing from the coronary sinus at a previously determined threshold rate in I1 patients. A dose of 0.05 to 0.1 mg NTG in 1 ml of 5% dextrose was then injected into the LCA. If the intensity of angina did not decrease or was increased, the pacing was discontinued after 1 minute. Arterial blood pressure, lead Vn and coronary sinus blood flow by thermodilution were recorded continuously. In ‘7 patients the same procedure was repeated with injection into the RCA. In none pf the patients did the injection of NTG into either coronary artery alleviate angina in spite of a significant increase in CSBF in 4 of them. NTG was ineffective whether injected into the obstructed artery or into the artery supplying collateral vessels to the obstructed artery. In 3 patients the injection of NTG into the LCA was followed after 60 seconds by intravenous injection of 0.3 mg NTG. The latter caused a significant decrease in blood pressure and in 1 to 2 minutes relieved the pain unaffected by the preceding intracoronary injection. The results indicate that the direct effects of NTG on the coronary arteries play little, if any, role in this agent’s antianginal action, which appears to be due entirely to the reduction of myocardial oxygen requirements, secondary to the agent’s effects on the systemic circulation. Electrophysiologic Properties of Atrial and Ventricular Muscle from Cats with Experimentally Induced Heart Failure and Hypertrophy HENRY GELBAND, MD*; ARTHUR L. BASSETT, PhD, New York, New York
Previously, we noted characteristic changes in ventricular electrical properties after chronic partial pulmonary arterial (PA) occlusion. To evaluate the role of altered electrical properties in development of right heart failure (RHF) and ventricular hypertrophy (RVH), we monitored action potentials (AP) and isometric force (P) of atria1 and ventricular muscle from normal, sham operated, RHF and RVH cats. Chronic right ventricular systolic hypertension produced by PA occlusion was followed by RVH and RHF. For right atria1 and right ventricular muscles from RHF cats, resting potential (RP) , AP amplitude, AP rate of rise, P and dP/dt were decreased compared to values in control muscles. Epinephrine and acetylcholine (ACh) in-
VOLUME
29, FEBRUARY
1972
creased RP, AP amplitude, AP rate of rise and P in failed atria1 muscles, whereas ACh increased RP but decreased P in normal atria1 muscles. These data indicate that depressed RP, AP amplitude and conduction may exacerbate the contractile defect in RHF. Right ventricular muscles removed from hearts (without failure) 1 day after PA banding had normal electrical and mechanical properties. Right ventricular muscles removed from hearts (without failure) 3 days after PA banding had depressed P and dP,/dt; electrical properties were normal except AP plateau was shifted to more negative potentials. Shift in level of AP plateau voltage was less for right ventricular muscles from ‘7 day bands. AP plateau voltage level was normal for right ventricular muscles 21 and 90 days after PA banding although P was still decreased. Altered voltage level for AP plateau may affect voltage-dependent contractile events and thus P in early stage of hypertrophy.
Thirty-Two Cases of Interventricular Septal Defect and Aortic Insufficiency: Clinical, Hemodynamic and Surgical Features STEPHEN P. GLASSER, MAJ, MC, USA*; MELVIN D. CHEITLIN, LTC, MC, USA, FACC; RICHARD J. MCCARTY, LTC, MC, USA, FACC; JOHN H. HAAS, LTC, MC, USA; ROBERT J. HALL, MD, FACC; CHARLES E. MULLINS, MD, Washington, D. C., San Francisco, California, El Paso, Texas, and Tacoma, Washington
Thirty-two cases of interventricular septal defect (IVSD) with aortic insufficiency (AI) are reported, in 20 of which operations were performed. The aortic insufficiency was generally slowly progressive in those patients in whom this could be determined. A right ventricular subpulmonic valvular gradient was found in 45% (13 patients), and in about half of these (6 patients) the gradient was due to prolapse and herniation of the right aortic cusp through the IVSD. This is a mu+ higher incidence than has been appreciated. Of the 20 patients operated upon, none had aortic valve replacement, 6 had accompanying annuloplaaties and 14 had IVSD closure only. In none was the aortic insufficiency made worse, and in only 5 was the AI definitely not benefited. In 3 cases of IVSD closure only, the AI completely disappeared postoperatively, and in at least 4 others the AI was significantly reduced in severity. It is concluded that patients with this combination of lesions should be considered for early closure of the IVSD in order to prevent progressive AI.
Augmentation of Contractility Following lschemia in the Isolated Supported Heart ROBERT E. GOLDSTEIN, MD*; JEFFREY S. BORER, MD; STEPHEN E. EPSTEIN, MD, Bethesda, Maryland Catecholamine-mediated increases in contractility have been observed immediately following release of coronary artery occlusion, an effect sometimes attributed to local release of myocardial norepinephrine stores. However, previous studies have not excluded the possibility that this inotropic effect may depend upon neural or humoral mechanisms. We therefore examined the influence of ischemia on contractile performance of completely isolated, working canine hearts. Coronary perfusion was maintained using arterial blood from a
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of the Wenckebach cycle is blocked retrograde is due to a collision of the reentrant and the retrograde wavefronts. A similar mechanism may explain antegrade Wenckebach. Failure of lntracoronary Pacing-Induced Angina
Nitroglycerin
to Alleviate
WILLIAM GANZ, MD, FACC*; HAROLD S. MARCUS, MD, Los Angeles, California
To assess the role of the direct effects of nitroglycerin (NTG) on the coronary circulation in the relief of angina, NTG was injected after induction of angina by pacing into the left (LCA) or right coronary artery (RCA) ; the doses were too small to cause a significant decrease in arterial blood pressure but in normal subjects were sufficient to augment coronary sinus blood flow (CSBF) by 50 to 100% for 30 to 60 seconds. After insertion of the angiographic catheter into the LCA, angina was induced by pacing from the coronary sinus at a previously determined threshold rate in I1 patients. A dose of 0.05 to 0.1 mg NTG in 1 ml of 5% dextrose was then injected into the LCA. If the intensity of angina did not decrease or was increased, the pacing was discontinued after 1 minute. Arterial blood pressure, lead Vn and coronary sinus blood flow by thermodilution were recorded continuously. In ‘7 patients the same procedure was repeated with injection into the RCA. In none pf the patients did the injection of NTG into either coronary artery alleviate angina in spite of a significant increase in CSBF in 4 of them. NTG was ineffective whether injected into the obstructed artery or into the artery supplying collateral vessels to the obstructed artery. In 3 patients the injection of NTG into the LCA was followed after 60 seconds by intravenous injection of 0.3 mg NTG. The latter caused a significant decrease in blood pressure and in 1 to 2 minutes relieved the pain unaffected by the preceding intracoronary injection. The results indicate that the direct effects of NTG on the coronary arteries play little, if any, role in this agent’s antianginal action, which appears to be due entirely to the reduction of myocardial oxygen requirements, secondary to the agent’s effects on the systemic circulation. Electrophysiologic Properties of Atrial and Ventricular Muscle from Cats with Experimentally Induced Heart Failure and Hypertrophy HENRY GELBAND, MD*; ARTHUR L. BASSETT, PhD, New York, New York
Previously, we noted characteristic changes in ventricular electrical properties after chronic partial pulmonary arterial (PA) occlusion. To evaluate the role of altered electrical properties in development of right heart failure (RHF) and ventricular hypertrophy (RVH), we monitored action potentials (AP) and isometric force (P) of atria1 and ventricular muscle from normal, sham operated, RHF and RVH cats. Chronic right ventricular systolic hypertension produced by PA occlusion was followed by RVH and RHF. For right atria1 and right ventricular muscles from RHF cats, resting potential (RP) , AP amplitude, AP rate of rise, P and dP/dt were decreased compared to values in control muscles. Epinephrine and acetylcholine (ACh) in-
VOLUME
29, FEBRUARY
1972
creased RP, AP amplitude, AP rate of rise and P in failed atria1 muscles, whereas ACh increased RP but decreased P in normal atria1 muscles. These data indicate that depressed RP, AP amplitude and conduction may exacerbate the contractile defect in RHF. Right ventricular muscles removed from hearts (without failure) 1 day after PA banding had normal electrical and mechanical properties. Right ventricular muscles removed from hearts (without failure) 3 days after PA banding had depressed P and dP,/dt; electrical properties were normal except AP plateau was shifted to more negative potentials. Shift in level of AP plateau voltage was less for right ventricular muscles from ‘7 day bands. AP plateau voltage level was normal for right ventricular muscles 21 and 90 days after PA banding although P was still decreased. Altered voltage level for AP plateau may affect voltage-dependent contractile events and thus P in early stage of hypertrophy.
Thirty-Two Cases of Interventricular Septal Defect and Aortic Insufficiency: Clinical, Hemodynamic and Surgical Features STEPHEN P. GLASSER, MAJ, MC, USA*; MELVIN D. CHEITLIN, LTC, MC, USA, FACC; RICHARD J. MCCARTY, LTC, MC, USA, FACC; JOHN H. HAAS, LTC, MC, USA; ROBERT J. HALL, MD, FACC; CHARLES E. MULLINS, MD, Washington, D. C., San Francisco, California, El Paso, Texas, and Tacoma, Washington
Thirty-two cases of interventricular septal defect (IVSD) with aortic insufficiency (AI) are reported, in 20 of which operations were performed. The aortic insufficiency was generally slowly progressive in those patients in whom this could be determined. A right ventricular subpulmonic valvular gradient was found in 45% (13 patients), and in about half of these (6 patients) the gradient was due to prolapse and herniation of the right aortic cusp through the IVSD. This is a mu+ higher incidence than has been appreciated. Of the 20 patients operated upon, none had aortic valve replacement, 6 had accompanying annuloplaaties and 14 had IVSD closure only. In none was the aortic insufficiency made worse, and in only 5 was the AI definitely not benefited. In 3 cases of IVSD closure only, the AI completely disappeared postoperatively, and in at least 4 others the AI was significantly reduced in severity. It is concluded that patients with this combination of lesions should be considered for early closure of the IVSD in order to prevent progressive AI.
Augmentation of Contractility Following lschemia in the Isolated Supported Heart ROBERT E. GOLDSTEIN, MD*; JEFFREY S. BORER, MD; STEPHEN E. EPSTEIN, MD, Bethesda, Maryland Catecholamine-mediated increases in contractility have been observed immediately following release of coronary artery occlusion, an effect sometimes attributed to local release of myocardial norepinephrine stores. However, previous studies have not excluded the possibility that this inotropic effect may depend upon neural or humoral mechanisms. We therefore examined the influence of ischemia on contractile performance of completely isolated, working canine hearts. Coronary perfusion was maintained using arterial blood from a
265