Myocardial Demand Research Articles

Angina Pectoris— Mechanism and Treatment

To the Editor:— The clinical study of angina pectoris reveals that all cardiovascular signs are signs of sympathetic overactivity, such as tachycardia, increase of blood pressure, arterial hypertonia, or increase of myocardial demands. The sympathetic system also exerts a coronary vasodilation action. The overactivity of the sympathetic system in angina pectoris explains why the drugs useful here are sympatholytics or antiadrenergics and the new treatments of this disease (propranolol hydrochloride and the electric stimulation of the carotid sinus) provide the same action. The good results published by Wasserman in 1928 through mechanical stimulation of the carotid sinus have been amply confirmed. 1 The carotid sinus stimulation may have resulted in a decrease of the sympathetic activity or in an increase of vagal activity. 2 Wasserman wondered how it is possible to reduce the anginal pain when the resultant vagal stimulation produces a coronary vasoconstriction. The explanation is that the vagal

Immediate revascularization of the heart.

The surgical treatment of myocardial ischemia demands immediate revascularization. In 70 patients this demand was met by the use of 114 aorta-to-coronary artery saphenous vein bypass grafts. Thirty-four single, 28 double, and 8 triple bypass grafts were used. They were taken to the right coronary artery (38 times), to the left anterior descending coronary artery (60 times), and to the circumflex coronary artery (16 times). There were 28 patients with three-vessel coronary disease (stenosis greater than 75%) and 15 with two-vessel disease. In spite of this, the operative mortality was only 10% (7 of 70), and four patients died of their disease while awaiting surgery. Relief of symptoms, which occurs without delay, has continued in 81% of the patients (57 of 70). The use of aorta-to-coronary artery saphenous vein bypass grafts "jump grafts" is proposed as being widely applicable, very effective, and the safest procedure available for the surgical treatment of coronary artery occlusive disease. More observations on longterm results are still needed.

Propranolol in Angina Pectoris

To the Editor:— The anginal pains in pheochromocytoma raises the question of the mechanism of this pain during the release of sympathetic neurohormones (epinephrine and norepinephrine) which are coronary dilators. These adrenergic neurohormones produce at the same time an increase in myocardial demands (the catabolic action of the sympathetic) to a greater degree than is met by the increased blood supply. The insufficient increase of blood supply related to the myocardial needs is also the cause of angina pectoris in patients with coronary artery disease. This catabolic action of the sympathetic nervous system and the insufficient increase in blood supply are signs of sympathetic overactivity, but other cardiovascular signs of angina pectoris are related to this overactivity such as tachycardia, increase of blood pressure, and arterial hypertonia. Overactivity of the sympathetic in anginal attacks explains why drugs useful here are sympatholytics, including the beta-adrenergic blocking agent, propranolol hydrochloride. This explains

The Effect of Glucagon on the Coronary Circulation in Man

Glucagon, 300 µg/ minute, was infused intravenously over 15 minutes in 27 subjects. The patients were divided into three groups: group I, patients without heart disease; group II, patients with arteriosclerotic heart disease; and group III, patients with congestive heart failure. Hemodynamic measurements included observations on myocardial blood flow using bolus injections of 84 rubidium and a coincidence counting technic. Myocardial oxygen consumption was determined after coronary sinus intubation in nine of the 27 patients. Significant increases were noted in heart rate, mean arterial pressure, tension-time index/minute and left ventricular work. Myocardial blood flow increased significantly while myocardial oxygen extraction remained constant suggesting that the augmentation in blood flow was sufficient to meet the increased myocardial demands for oxygen. The effects of glucagon on the coronary circulation resemble that of isoproterenol rather than norepinephrine without, however, leading to the production of arrhythmias seen with these catecholamines.

Effect of 1-epinephrine on the coronary circulation in human subjects with and without coronary artery disease.

The effects of intravenous infusion of epinephrine on the coronary circulation of 21 human subjects, 8 with and 13 without coronary artery disease, have been studied. The response to epinephrine was similar in the two groups. Epinephrine increased cardiac output, stroke volume, and systolic ejection rate significantly without significant change in blood pressure. Myocardial O 2 consumption increased in relation to increased kinetics of contraction. Coronary flow increased significantly without change in coronary arteriovenous O 2 difference, suggesting that the vasodilatory response to epinephrine in man is secondary to augmented myocardial metabolic demands.

The oxygen supply of the human heart ∗

The factors involved in oxygenation of the human heart have been discussed and illustrated in normal subjects and in common forms of heart disease. Within all groups at rest, significant variability in ventricular performance, myocardial oxygen requirements and oxygen supply patterns exists, suggesting that individual resting observations are of little value in detecting abnormalities of the coronary circulation. An exception appears to exist in low cardiac output congestive heart failure where functional coronary insufficiency is postulated due to coronary participation in peripheral vasoconstriction. During exercise, increased myocardial oxygen requirements are met by elevated coronary blood flow in normal coronary subjects, allowing maintenance of resting myocardial oxygen tension. Coronary vascular reserve is inadequate in coronary arterial disease, and a compensatory elevation of myocardial oxygen extraction lowers exercise coronary venous oxygen saturation and, presumably, myocardial oxygen tension. In congestive heart failure, markedly elevated exercise myocardial oxygen requirements place extraordinary demands on the coronary circulation, and in some instances may precipitate insufficiency of the anatomically normal or mildly diseased coronary circulation. An important consequence of coronary insufficiency appears to be compensatory elevation of myocardial oxygen extraction and reduction of myocardial oxygen tension during exercise. These studies demonstrate no relationship between absolute coronary venous oxygen values and angina pectoris, although the precipitation of this symptom may be related to the degree of reduction in coronary venous oxygenation during exercise. Analysis of myocardial lactate, pyruvate and catecholamine metabolism reveals no causal relationship to angina pectoris or coronary vasodilatation. Of the study subjects having angina pectoris, 82 per cent have detectable oxygen supply abnormalities, an incidence in close agreement with that of diffuse versus localized coronary arterial disease. The role of inefficient energy utilization has been suggested in the precipitation of coronary insufficiency in congestive heart failure and obliterative coronary arterial disease. Conversely, reduced myocardial oxygen tension secondary to coronary insufficiency may impair ventricular performance and result in myocardial damage. These problems require further evaluation of the biochemical events associated with coronary insufficiency, and an examination of myocardial energy production and utilization in coronary arterial disease.

Effects of a new coronary vasodilator on the general and coronary hemodynamics and myocardial metabolism of man.

Article1 July 1959EFFECTS OF A NEW "CORONARY VASODILATOR" ON THE GENERAL AND CORONARY HEMODYNAMICS AND MYOCARDIAL METABOLISM OF MANELMERICE TRAKS, M.D., DONALD B. HACKEL, M.D., SALVATORE M. SANCETTA, M.D., F.A.C.P.ELMERICE TRAKS, M.D.Search for more papers by this author, DONALD B. HACKEL, M.D.Search for more papers by this author, SALVATORE M. SANCETTA, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-51-1-31 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe continued pharmacologic search for drugs capable of producing a positive increase in the coronary blood of man is an important phase in the management of patients with coronary artery disease. It is a distressing fact that many substances which pharmacologically appear to be promising later fail to fulfill this promise in the course of direct clinical trial. The clinical use of such "vasodilator" substances is often predicated upon the physiologic observation that they produce an increased coronary blood flow in animal preparations, without considering the possibility that the increase in flow may represent solely a heightened myocardial demand induced...Bibliography1. AhlquistHobentachWoodbury RPBRA: A pharmacologic study of N-methyl-N-cinnamyl-2-phenyl-propylamine, J. Am. Pharm. A. (Scient. Ed.) 38: 425, 1949. CrossrefGoogle Scholar2. BarkerSummerson SBWH: The colorimetric determination of lactic acid in biological material, J. Biol. Chem. 138: 535, 1948. CrossrefGoogle Scholar3. DaviesBrink PWF: Microelectrodes for measuring oxygen tension in animal tissues, Rev. Scient. Instruments 13: 524, 1942. CrossrefGoogle Scholar4. EckenhoffHafkenschiel JEJH: The effect of nikethamide on coronary blood flow and cardiac oxygen metabolism, J. Pharmacol. and Exper. Therap. 91: 362, 1947. MedlineGoogle Scholar5. EckenhoffHafkenschielLandmesser JEJHCM: The coronary circulation in the dog, Am. J. Physiol. 148: 582, 1947. CrossrefMedlineGoogle Scholar6. EckenhoffHafkenschielLandmesserHarmel JEJHCMM: Cardiac oxygen metabolism and control of the coronary circulation, Am. J. Physiol. 149: 634, 1947. CrossrefMedlineGoogle Scholar7. FoltzRubinSteigerGazes ELAWADC: The effects of intravenous aminophylline upon the coronary blood-oxygen exchange, Circulation 2: 215, 1950. CrossrefMedlineGoogle Scholar8. FriedemannHaugen TEGE: Pyruvic acid determination of keto acids in blood and urine, J. Biol. Chem. 147: 415, 1943. CrossrefGoogle Scholar9. GoodaleHackel WTDB: Measurement of coronary blood flow in dogs and man from rate of myocardial nitrous oxide desaturation, Circul. Res. 1: 502, 1953. CrossrefMedlineGoogle Scholar10. GoodaleLubinEckenhoffHafkenschielBanfield WTHJEJHWG: Coronary sinus catheterization for studying coronary blood flow and myocardial metabolism, Am. J. Physiol. 152: 340, 1948. CrossrefMedlineGoogle Scholar11. KienGomollSherrod GAAWTR: Coronary vasodilator action of cinnamyl vonedrine, Federation Proc. 15: 446, 1956. Google Scholar12. SilberKatz ENLN: Coronary dilators and angina. Reappraisal, J. A. M. A. 153: 1075, 1953. CrossrefMedlineGoogle Scholar13. Somogyi M: Determination of blood sugar, J. Biol. Chem. 160: 69, 1945. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cleveland, Ohio*Received for publication September 15, 1958.From the Departments of Medicine and Pathology, Cleveland Metropolitan General Hospital and Western Reserve University, Cleveland, Ohio.†With the technical assistance of GLADYS HECKMAN, R. N., HANNA JANOUSKOVEC, R. N., and EDNA STONE, A. B., Cleveland, Ohio.Supported by grants from the U. S. Public Health Service (H-863) (Dr. Hackel), The William S. Merrell Co., and the Cleveland Area Heart Society (Dr. Sancetta), and performed in part during tenure of a Research Fellowship from the American Heart Association (Dr. Traks).‡Vasoflex is the trademark of the Wm. S. Merrell Co., Cincinnati, Ohio. It was supplied as a parenteral solution containing 5 mg./ml.Requests for reprints should be addressed to Elmerice Traks, M.D., Cleveland Metropolitan General Hospital, 3395 Scranton Road, Cleveland 9, Ohio. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySYMPATHOMIMETIC DRUGSIsoproterenol and cardiovascular performancePROBLEMS IN THE TREATMENT OF DECOMPRESSION SICKNESS (AND TRAUMATIC AIR EMBOLISM)Bibliography 1 July 1959Volume 51, Issue 1Page: 31-38KeywordsClinical trialsCoronary arteriesDrugsFellowshipsHeartHemodynamicsHospital medicineMedical servicesStable coronary artery diseaseVasodilators ePublished: 1 December 2008 Issue Published: 1 July 1959 PDF downloadLoading ...

The Surgical Treatment of Coronary Insufficiency

1. The surgical procedures devised for the treatment of coronary arterial insufficiency may be classified according to the objectives they seek to accomplish. 2. Measures which modify only the clinical manifestations of the coronary arterial insufficiency consist of those which destroy the sympathetic pathways mediating pain sensation from the heart by postganglionic resection of the upper dorsal and lower cervical chains, by division of the preganglionic fibers to these same areas, or by paravertebral injections of alcohol. 3. The only available method which modifies the degree of coronary insufficiency by decreasing myocardial demand is destruction of thyroid function by surgical or medical therapy. 4. Coronary insufficiency may be decreased by a variety of procedures which are designed to increase the size of the coronary vascular bed. These are best termed revascularization techniques, and represent the most physiological approach to the problem. They are classified according to their ability to increase the vascularity at a superficial level or throughout all layers of the myocardium. 5. The blood supply to the epicardium, or the layers immediately beneath the epicardium, may be augmented by omentopexy, myopexy, pneumonopexy, the intrapericardial insufflation of irritants, or the implantation of the bleeding end of the mobilized left internal mammary artery into the left ventricular wall. The intrapericardial instillation of a powdered silicate appears to be the most promising of the surface revascularization procedures. 6. The term total revascularization is applied to the techniques which create an anastomsis between the aorta and the coronary sinus either through a vascular graft (Beck II) or directly (Kralik modification) thus establishing a retrograde flow of arterial blood to the myocardial capillary bed by way of the venous channels. Such retrograde flow is transient but great augmentation of the adequacy of the intercoronary collateral system is produced and remains. Simple ligation of the coronary sinus also may be considered as a total revascularization procedure although a lesser degree of intercoronary overdevelopment is obtained by this procedure. 7. The selection of patients for the revascularization procedures is based upon those manifestations of the disease which indicate an ominous prognosis or seriously interfere with the ability of the patient to meet the requirements of ordinary living. 8. Resection of a ventricular aneurysm represents a promising surgical development in the management of a relatively recalcitrant and untoward cardiac complication which nearly always is the result of occlusive coronary arterial disease. The first historically successful case is herein presented. 9. The development of a seemingly satisfactory and rather safe surgical treatment for complete or varying heart block is detailed with presentation of the first apparently successful human operation.