- Email: [email protected]
The intermediate coronary care unit (ICCU)
ABSTRACTS
have been inconsistent. In cats, experimental pulmonary arterial stenosis was associated with increased collagen in both ventricles. However, in none of these studies was increased collagen formation proven to be related to hypertrophy per se. The Syrian hamster with a hereditary cardiomyopathy offers a unique opportunity to study the relation of collagen content and hypertrophy. A spontaneous cardiomyopathy with lysis of cells occurs between 30 to 60 days of life with subsequent healing. After about 120 days, hypertrophy develops, which is complete by 300 days. Eventually congestive heart failure and death ensue. Accordingly, myocardial hydroxyproline was determined to provide a measure of collagen. At 120 days hydroxyproline concentration was already increased from 1.17 pg/mg dry weight of heart in normal animals (N) to 2.84 ? 0.302 (1 SD) in the myopathic animals (M) ,and did not increase further by 300 days despite
Effects of Glucagon on Contractility and Adenylcyclase Activity of Human Papillary Muscles ROBERT E. GOLDSTEIN, MD; C. LYNN SKELTON, S. LEVEY. MD: D. LUKE GLANCY. MD: G. DAVID STEPHEN E. EPSTEIN, MD, Bethesda, Maryland
MD; GERALD BEISER, MD;
Glucagon (G) exerts positive inotropic effects in normal hearts but is ineffective in animals with chronic cardiac failure. To assess directly the influence of G on human myocardium, we measured contractility and activation of adenylcyclase (AC), the enzyme thought to mediate the inotropic action of G, in left ventricular papillary muscles (PM) obtained from 13 patients at mitral valve replacement. On the basis of preoperative ventricular end-diastolic pressures and cardiac output (independent of PM data) patients were classified in 3 groups: normal, with cardiac failure or indeterminate. Concentration-response curves showed that G caused a mean 12% rise in peak PM tension and 13% rise in peak rate of tension development in the 4 normal patients. AC activity in PM from each normal patient rose after G (average = 830/r, P
26.
DECEMBER
1970
associated activation of AC after G, perhaps explaining the inefficacy of this drug in treating patients with chronic cardiac failure.
The First Hour in Acute Myocardial Infarction (AMI): Observations on 50 Patients WILLIAM J. GRACE, New York, New York
MD,
FACC; JOHN
A. CHADBOURN,
MD,
Fifty consecutive patients with acute myocardial in.farction were seen by the mobile coronary care unit (MCCU) team within 1 hour after onset of chest pain. Continuous electrocardiographic monitoring was started outside of the hospital in all. The arrhythmias encountered were premature ventricular contractions (5), atria1 flutter (2), sinus bradycardia (4)) atrioventricular (A-V) dissociation (2), ventricular tachycardia (1)) sinoatrial block (1)) supraventricular tachycardia (I) and ventricular fibrillation (VF) (2). A temporary pacemaker was required in 3 patients. Arrhythmias were treated at the site. The 2 patients with VF were successfully defibrillated outside of the hospital. Three of these 50 patients died during the subsequent hospital course. The causes of death were intractable ventricular fibrillation (1)) refractory congestive heart failure (1) and A-V dissociation with ventricular standstill (1). Hospital mortality in these patients was 3 of 50 (6 % ) . Hospital mortality rate of patients seen after more than 2 hours of chest pain in the MCCU was 20%. Absence of the usual type of shock syndrome was notable. Constant monitoring, treatment for arrhythmia, oxygen and medication for pain seem to result in a significant lowering of the mortality rate if provided in the early stages of AMI.
The Intermediate Coronary Care Unit (ICCU) WILLIAM J. GRACE, New York, New York
MD,
FACC;
PATRICIA
M. YARVOTE,
MD,
After discharge from a coronary care unit (CCU) a number of patients die. As many as 30% of all the hospital deaths from acute myocardial infarction (AMI) occur after the sixth day or after discharge from the CCU. In our experience at least half of these deaths are sudden and unexpected. To study the problem a special area in the general hospital was equipped for continuous electrocardiographic (ECG) monitoring using teIemetry. The area was also equipped with the usual life support measures in the event of cardiac arrest, and the assigned nurses were given special courses in ECG techniques and resuscitation. To date over 200 patients with transmural infarction have been treated in this ICCU. The average stay was 12 days. On the basis of retrospective analysis of our data we anticipated 1 death per month. In an 18 month period there have been 2 deaths in the ICCU. One death was due to recurrent atrioventricular block in a patient who had previously been resuscitated. The second death was sudden and unexpected and occurred while the patient was dressing just before discharge. Two other deaths occurred from congestive heart failure in patients who were returned to the CCU from the ICCU. In the past
635
ABSTRACTS
17 months there has been only 1 death in this unit. Eight percent of patients were returned to the CCU for control of recurrent arrhythmia. An additional 5% were returned to the CCU for recurrence of chest pain. These data suggest that continuous ECG monitoring beyond the time generally provided for in a CCU is a necessary part of the overall hospital plan for care of a patient with acute myocardial infarction and is a necessary adjunct if the mortality from acute myocardial infarction is to be further reduced.
2-O Interval as an Indicator of Left Atrial Pressure WAYNE Kansas
GRAY,
MD;
HUBERT
H. BELL,
Jr.,
MD,
Kansas
City,
The time interval between aortic closure sound and the 0 point of the apex cardiogram (2-O interval) was determined in a group of 30 normotensive patients by standard phonocardiographic technique. The 2-O interval was then correlated with mean left atria1 or pulmonary arterial wedge pressure obtained at cardiac catheterization. The correlation coefficient was -0.73. Fifteen patients had evidence of cardiac decompensation and were found to have severe coronary artery or myocardial disease. Mean left atria1 or wedge pressure ranged from 15 to 32 mm Hg (average 19 mm Hg) and the 2-O interval ranged from 0.10 to 0.06 second (average 0.07 second). A 2-O interval of 0.07 second or less was associated with a left atria1 pressure of 18 mm Hg or greater. A 2-O interval of 0.06 second or less was associated with a left atria1 pressure of 24 mm Hg or greater. Fifteen patients had no evidence of cardiac disease. Mean left atria1 or wedge pressure ranged from 3 to 11 mm Hg (average 7 mm Hg) and the 2-O interval ranged from 0.14 to 0.08 second (average 0.09 second). The 2-O interval is a simple, accurate, noninvasive method of estimating left atria1 pressure.
Sinus Node, Potassium and Sympathetic System J. GREINEDER, MD; JACKSON H. STUCKEY, SALLE, MD, Brooklyn, New York
MD; MARIO
Absence of Bowditch Phenomenon in the Ventricular Muscle of Hamsters with Hereditary Cardiomyopathy STEPHEN Bethesda,
HAJDU, Maryland
MD;
CHRISTIAN
J.
POSNER,
MD,
PhD,
The interval-tension relation of right ventricular muscles of normal hamsters was compared to that of hamsters with hereditary cardiomyopathy, with or without congestive heart failure. The contractility of the heart of cardiomyopathic animals without circulatory insufficiency did not differ from that of the normal animals at any frequency. The cardiac muscle of animals with severe congestive heart failure showed normal contractility at a low frequemy of stimulation (range of the Woodworth phenomenon) but did not show the increased contractility upon high frequency stimulation (Bowditch phenomenon) seen in all other animals. Ryanodine, which eliminates only the contractility caused by the Woodworth phenomenon, abolished the contractility of the hearts of animals with congestive failure over the whole frequency range. Cardiac glycosides, which are known to potentiate the Bowditch phenomenon, were ineffective on the cardiac muscle of animals without Bowditch phenomenon. The probable cause of cardiac failure in hamsters with hereditary cardiomyopathy is discussed.
VAS-
Catecholamines counteract the depressant action of POtassium (K) on cardiac excitability. This elicits the question whether they also counteract the depressant action of this ion on cardiac automaticity. Thus, the sinus node is both particularly resistant to high concentrations of K and is heavily innervated by sympathetic fibers. This question was investigated in anesthetized dogs in which the sinus nodal artery was perfused with Tyrode solution containing different amounts of K and had electrodes sutured at different locations in the atria. In most dogs with autonomic innervation intact, sinus rhythm persisted even when [K], = 21.6 mEq/ liter. A role of vagal withdrawal in this resistance to high level of K was ruled out by bilateral vagotomy. Acute sympathectomy (bilateral section of stellate ganglia and first 5 thoracic ganglia) resulted in the disappearance of the sinoatrial (SA) rhythm in some of the animals with [K], = 21.6 mEq/liter. Administration of propranolol resulted in the loss of sinus
636
nodal rhythm when K was increased to the highest level. The same results were obtained with previous administration of reserpine and also in animals with chronic sympathectomy. To study the shift in pacemaker, an electrode was sutured inside the right atrium near the atrioventricular (A-V) node. By the temporal relation of the electrograms recorded from SA node, right atrium, base of the right atrium and A-V nodal areas, it was found that under the experimental conditions high levels of K shift the pacemaker from the sinus node toward the atrioventricular node. These data suggest that the resistance of the sinus node to high levels of K is in part related to the presence of stores of catecholamine in the sinus nodal area. Possibly, high levels of K release these catecholamine stores directly.
Total Body Fluids and Electrolytes in Cardiac Failure CARLOS E. HARRISON, Rochester, Minnesota
MD,
PhD,
FACC;
L. P. NOVAK,
PhD,
Recent investigation demonstrated cardiac cellular abnormalities in animals with a 25% reduction of intracellular potassium (Harrison, Novak, et al. J Lab & Clin Med 75 :185, 1970). The objective of the present study was to assess the magnitude of cellular cation deficit in uncompensated and compensated human cardiac failure. Ten patients with uncompensated and 4 with compensated failure received 100 PC 42K, 50 PC 24Na and 50 ml D,O. Total body water (TBW), extracellular water (ECW), intracellular water (ICW), exchangeable potassium (K,) and exchangeable sodium (Na,) were determined by standard dilution principles, and intracellular potassium (ICK) concentration was calculated. These data were compared to predicted
The
American
Journal
of
CARDIOLOGY
have been inconsistent. In cats, experimental pulmonary arterial stenosis was associated with increased collagen in both ventricles. However, in none of these studies was increased collagen formation proven to be related to hypertrophy per se. The Syrian hamster with a hereditary cardiomyopathy offers a unique opportunity to study the relation of collagen content and hypertrophy. A spontaneous cardiomyopathy with lysis of cells occurs between 30 to 60 days of life with subsequent healing. After about 120 days, hypertrophy develops, which is complete by 300 days. Eventually congestive heart failure and death ensue. Accordingly, myocardial hydroxyproline was determined to provide a measure of collagen. At 120 days hydroxyproline concentration was already increased from 1.17 pg/mg dry weight of heart in normal animals (N) to 2.84 ? 0.302 (1 SD) in the myopathic animals (M) ,and did not increase further by 300 days despite
Effects of Glucagon on Contractility and Adenylcyclase Activity of Human Papillary Muscles ROBERT E. GOLDSTEIN, MD; C. LYNN SKELTON, S. LEVEY. MD: D. LUKE GLANCY. MD: G. DAVID STEPHEN E. EPSTEIN, MD, Bethesda, Maryland
MD; GERALD BEISER, MD;
Glucagon (G) exerts positive inotropic effects in normal hearts but is ineffective in animals with chronic cardiac failure. To assess directly the influence of G on human myocardium, we measured contractility and activation of adenylcyclase (AC), the enzyme thought to mediate the inotropic action of G, in left ventricular papillary muscles (PM) obtained from 13 patients at mitral valve replacement. On the basis of preoperative ventricular end-diastolic pressures and cardiac output (independent of PM data) patients were classified in 3 groups: normal, with cardiac failure or indeterminate. Concentration-response curves showed that G caused a mean 12% rise in peak PM tension and 13% rise in peak rate of tension development in the 4 normal patients. AC activity in PM from each normal patient rose after G (average = 830/r, P
26.
DECEMBER
1970
associated activation of AC after G, perhaps explaining the inefficacy of this drug in treating patients with chronic cardiac failure.
The First Hour in Acute Myocardial Infarction (AMI): Observations on 50 Patients WILLIAM J. GRACE, New York, New York
MD,
FACC; JOHN
A. CHADBOURN,
MD,
Fifty consecutive patients with acute myocardial in.farction were seen by the mobile coronary care unit (MCCU) team within 1 hour after onset of chest pain. Continuous electrocardiographic monitoring was started outside of the hospital in all. The arrhythmias encountered were premature ventricular contractions (5), atria1 flutter (2), sinus bradycardia (4)) atrioventricular (A-V) dissociation (2), ventricular tachycardia (1)) sinoatrial block (1)) supraventricular tachycardia (I) and ventricular fibrillation (VF) (2). A temporary pacemaker was required in 3 patients. Arrhythmias were treated at the site. The 2 patients with VF were successfully defibrillated outside of the hospital. Three of these 50 patients died during the subsequent hospital course. The causes of death were intractable ventricular fibrillation (1)) refractory congestive heart failure (1) and A-V dissociation with ventricular standstill (1). Hospital mortality in these patients was 3 of 50 (6 % ) . Hospital mortality rate of patients seen after more than 2 hours of chest pain in the MCCU was 20%. Absence of the usual type of shock syndrome was notable. Constant monitoring, treatment for arrhythmia, oxygen and medication for pain seem to result in a significant lowering of the mortality rate if provided in the early stages of AMI.
The Intermediate Coronary Care Unit (ICCU) WILLIAM J. GRACE, New York, New York
MD,
FACC;
PATRICIA
M. YARVOTE,
MD,
After discharge from a coronary care unit (CCU) a number of patients die. As many as 30% of all the hospital deaths from acute myocardial infarction (AMI) occur after the sixth day or after discharge from the CCU. In our experience at least half of these deaths are sudden and unexpected. To study the problem a special area in the general hospital was equipped for continuous electrocardiographic (ECG) monitoring using teIemetry. The area was also equipped with the usual life support measures in the event of cardiac arrest, and the assigned nurses were given special courses in ECG techniques and resuscitation. To date over 200 patients with transmural infarction have been treated in this ICCU. The average stay was 12 days. On the basis of retrospective analysis of our data we anticipated 1 death per month. In an 18 month period there have been 2 deaths in the ICCU. One death was due to recurrent atrioventricular block in a patient who had previously been resuscitated. The second death was sudden and unexpected and occurred while the patient was dressing just before discharge. Two other deaths occurred from congestive heart failure in patients who were returned to the CCU from the ICCU. In the past
635
ABSTRACTS
17 months there has been only 1 death in this unit. Eight percent of patients were returned to the CCU for control of recurrent arrhythmia. An additional 5% were returned to the CCU for recurrence of chest pain. These data suggest that continuous ECG monitoring beyond the time generally provided for in a CCU is a necessary part of the overall hospital plan for care of a patient with acute myocardial infarction and is a necessary adjunct if the mortality from acute myocardial infarction is to be further reduced.
2-O Interval as an Indicator of Left Atrial Pressure WAYNE Kansas
GRAY,
MD;
HUBERT
H. BELL,
Jr.,
MD,
Kansas
City,
The time interval between aortic closure sound and the 0 point of the apex cardiogram (2-O interval) was determined in a group of 30 normotensive patients by standard phonocardiographic technique. The 2-O interval was then correlated with mean left atria1 or pulmonary arterial wedge pressure obtained at cardiac catheterization. The correlation coefficient was -0.73. Fifteen patients had evidence of cardiac decompensation and were found to have severe coronary artery or myocardial disease. Mean left atria1 or wedge pressure ranged from 15 to 32 mm Hg (average 19 mm Hg) and the 2-O interval ranged from 0.10 to 0.06 second (average 0.07 second). A 2-O interval of 0.07 second or less was associated with a left atria1 pressure of 18 mm Hg or greater. A 2-O interval of 0.06 second or less was associated with a left atria1 pressure of 24 mm Hg or greater. Fifteen patients had no evidence of cardiac disease. Mean left atria1 or wedge pressure ranged from 3 to 11 mm Hg (average 7 mm Hg) and the 2-O interval ranged from 0.14 to 0.08 second (average 0.09 second). The 2-O interval is a simple, accurate, noninvasive method of estimating left atria1 pressure.
Sinus Node, Potassium and Sympathetic System J. GREINEDER, MD; JACKSON H. STUCKEY, SALLE, MD, Brooklyn, New York
MD; MARIO
Absence of Bowditch Phenomenon in the Ventricular Muscle of Hamsters with Hereditary Cardiomyopathy STEPHEN Bethesda,
HAJDU, Maryland
MD;
CHRISTIAN
J.
POSNER,
MD,
PhD,
The interval-tension relation of right ventricular muscles of normal hamsters was compared to that of hamsters with hereditary cardiomyopathy, with or without congestive heart failure. The contractility of the heart of cardiomyopathic animals without circulatory insufficiency did not differ from that of the normal animals at any frequency. The cardiac muscle of animals with severe congestive heart failure showed normal contractility at a low frequemy of stimulation (range of the Woodworth phenomenon) but did not show the increased contractility upon high frequency stimulation (Bowditch phenomenon) seen in all other animals. Ryanodine, which eliminates only the contractility caused by the Woodworth phenomenon, abolished the contractility of the hearts of animals with congestive failure over the whole frequency range. Cardiac glycosides, which are known to potentiate the Bowditch phenomenon, were ineffective on the cardiac muscle of animals without Bowditch phenomenon. The probable cause of cardiac failure in hamsters with hereditary cardiomyopathy is discussed.
VAS-
Catecholamines counteract the depressant action of POtassium (K) on cardiac excitability. This elicits the question whether they also counteract the depressant action of this ion on cardiac automaticity. Thus, the sinus node is both particularly resistant to high concentrations of K and is heavily innervated by sympathetic fibers. This question was investigated in anesthetized dogs in which the sinus nodal artery was perfused with Tyrode solution containing different amounts of K and had electrodes sutured at different locations in the atria. In most dogs with autonomic innervation intact, sinus rhythm persisted even when [K], = 21.6 mEq/ liter. A role of vagal withdrawal in this resistance to high level of K was ruled out by bilateral vagotomy. Acute sympathectomy (bilateral section of stellate ganglia and first 5 thoracic ganglia) resulted in the disappearance of the sinoatrial (SA) rhythm in some of the animals with [K], = 21.6 mEq/liter. Administration of propranolol resulted in the loss of sinus
636
nodal rhythm when K was increased to the highest level. The same results were obtained with previous administration of reserpine and also in animals with chronic sympathectomy. To study the shift in pacemaker, an electrode was sutured inside the right atrium near the atrioventricular (A-V) node. By the temporal relation of the electrograms recorded from SA node, right atrium, base of the right atrium and A-V nodal areas, it was found that under the experimental conditions high levels of K shift the pacemaker from the sinus node toward the atrioventricular node. These data suggest that the resistance of the sinus node to high levels of K is in part related to the presence of stores of catecholamine in the sinus nodal area. Possibly, high levels of K release these catecholamine stores directly.
Total Body Fluids and Electrolytes in Cardiac Failure CARLOS E. HARRISON, Rochester, Minnesota
MD,
PhD,
FACC;
L. P. NOVAK,
PhD,
Recent investigation demonstrated cardiac cellular abnormalities in animals with a 25% reduction of intracellular potassium (Harrison, Novak, et al. J Lab & Clin Med 75 :185, 1970). The objective of the present study was to assess the magnitude of cellular cation deficit in uncompensated and compensated human cardiac failure. Ten patients with uncompensated and 4 with compensated failure received 100 PC 42K, 50 PC 24Na and 50 ml D,O. Total body water (TBW), extracellular water (ECW), intracellular water (ICW), exchangeable potassium (K,) and exchangeable sodium (Na,) were determined by standard dilution principles, and intracellular potassium (ICK) concentration was calculated. These data were compared to predicted
The
American
Journal
of
CARDIOLOGY