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Phantom angina
Volume Number
116 6, Part 1
Brief
approach. A 5F wedge balloon catheter was advanced through the aortic valve into the right ventricle. The balloon was then inflated and the catheter was easily passed across the ventricular septal defect into the pulmonary artery. Case No. 3. (Fig. 2). A 2% -year-old girl had levotransposition of the great vessels, a double-inlet single left ventricle, subaortic outflow chamber, and valvular and subvalvular pulmonary stenosis. She had previously undergone a polytetrafluoroethylene interposition graft from the left subclavian artery to the pulmonary artery. Catheterization was performed 2 years after the shunt procedure to assess her pulmonary pressures and future Fontan procedure candidacy. Her previous anatomic findings were confirmed. The venous catheter could be advanced to the atrium and then to the ventricle, but it could not be advanced further into the pulmonary artery. This difficulty was encountered because of an interrupted inferior vena cava and hemiazygous venous continuation to the high right atrium. Thus a 5F Berman catheter was advanced via the aorta to the subaortic outflow chamber, across the bulboventricular foramen into the left ventricle to the subpulmonary area and thence to the pulmonary artery. Catheter entry into the pulmonary artery is often mandatory for obtaining adequate presurgical hemodynamic and anatomic information, especially when patients have complex forms of congenital heart disease. Catheter manipulation into the pulmonary artery from the venous approach is often possible, but is sometimes difficult or impossible when patients have various forms of single ventricle anatomy or physiology, especially in conjunction with malposed great vessels and associated pulmonary stenosis. Aberrations in systemic venous anatomy, either congenital or acquired, can also interfere with adequate catheter manipulation. Lock et al.’ described this technique for use in patients with double-outlet ventricles. In this communication, the concept is expanded to include patients with single ventricular anatomy and to those with large ventricular septal defects and various forms of transposition. The method of retrograde aortic passage of a balloon catheter into the ventricle, inflation of the balloon, and usually easy pulmonary artery entry in these sit,uations allows the cardiologist to obtain the necessary rnformation for proper surgical decision making. The above case examples each demonstrated situations where obtaining hemodynamic or anatomic information was essential. We were unable to enter the pulmonary artery by conventional means in any of them, but had no problems with the retrograde aortic technique. We have found the technique simple, uncomplicated, and thus recommend its application to situations such as those described above. REFERENCE
1. Lock JE, Keane JF, Fellows KE. Diagnostic tional catheterization in congenital heart Lancaster: Martinus Nijhoff, 1987:27.
and
intervendisease. Boston,
Phantom
Communications
1627
angina
Stephen W. Mester, MD, Guillermo B. Cintron, and Charles Long, MD.” Tampa, Flu.
MD,
In the 215 years since Sir William Heberden’s original description of angina pectoris, it has been difficult to find a more eloquent description of this “disorder of the breast . . .“I Exceptions to this description of what we now know to represent myocardial ischemia have probably been noted for 214 years. A feeling of the presence of or discomfort in a limb that has been amputated has been described previously as a phantom limb sensation.‘s3 Phantom limb sensation with angina1 quality has also been reported.4 We report a case of exertional myocardial ischemia presenting as a sensation of discomfort in the phantom hand of a previously amputated left upper extremity. This 62-year-old man suffered a traumatic left upper extremity amputation at the mid-humerus in 1944. Since that time, the patient had continuously noted the “presence” of his left hand, which appeared to arise directly from his medium-length, above elbow stump. He had no discomfort until 7 years ago, when he noted a sensation of pain in his absent left hand while operating his push lawn mower. This exertional discomfort forced the patient to change to a self-propelled mower and, finally, to a riding mower. Two years ago, the patient began noting this hand pain while taking his daily walk. The pain would be reliably reproduced with walking one-half mile and would be relieved promptly with rest, and was felt to be due to his above-elbow prosthesis. The pain gradually became more frequent and severe. Multiple evaluations of his humeral stump were performed, as were a surgical revision and corticosteroid injections of the stump, without resolution of his symptoms. When a trial of walking without the prosthesis reproduced the pain, the patient was suspected of having coronary artery disease and was referred for an exercise treadmill test. The patient had a IO-year history of arterial hypertension. There was no history of hypercholesterolemia, cigarette smoking, or family history of atherosclerotic disease. Physical examination revealed a blood pressure of 145/85 mm Hg and a pulse of 76 beats/min. A well-healed left mid-humeral stump was noted, and the remainder of the examination was unremarkable. The patient underwent exercise treadmill testing. He completed 4 minutes and 26 seconds of a Bruce protocol, achieving a heart rate of 131 beats/min (81% of predicted maximal heart rate) at a blood pressure of 176/75 mm Hg. The patient experienced the typical pain in his absent left hand at 3 minutes From the Division of Cardiology and the Medicine. University of South Florida College Haley Veterans Administration Hospital. Reprint Haley
requests: VA Hospital,
‘Division of Rehabilitation of Medicine and James
S. Mester, MD, Cardiology Section (111A). 13000 Bruce B. Downs Blvd., Tampa, FL
James 33612.
A. A.
1628
Brief
Communications
Fig. 1. Computerized electrocardiographic exercise exercise, and-at 4 and 8 minutes into recovery.
into the study and subsequently developed marked ST segment depression in the inferior and lateral leads (Fig. 1). Cardiac catheterization was performed and revealed a 60% left main coronary artery stenosis, a 95% proximal left anterior descending coronary artery stenosis, a 95% first diagonal branch ostial stenosis, a 60% proximal circumflex stenosis (codominant circulation), and an 80% proximal right coronary artery stenosis. The patient underwent surgical coronary revascularization and has returned to his usual activities without recurrence of his symptoms. During repeat exercise treadmill testing, the patient completed stage 2 of a Bruce protocol, achieving a heart rate of 135 beatslmin at a blood pressure of 200175 mm Hg. The patient had no pain or electrocardiographic (ECG) changes consistent with ischemia. A sensation of “phantom limb pain” in a previously amputated limb has been reported previously. The neurologic basis for this pain is unclear; there is also an incomplete understanding of the mechanisms of angina. From the heart, afIerent nerve fibers run to the spinal cord through cardiac nerves, the upper five thoracic sympathetic ganglia, the white rami communicantes (and to a minor extent, the grey), and the upper five thoracic dorsal roots. Impulses are then transmitted through the cord to the thalamus and on to the cerebral cortex.6 In the spinal cord, some impulses mediated by the with sympathetic tierent pathway may converge impulses from somatic thoracic structures onto the same ascending spinal neurons. This may explain referred cardiac pain.6 Pain impulses may be referred to the medial aspects of the arm via common connections through the L---l . 1 &aua. UI uc*IIcu We hypothesize that these connections are a factor in this patient’s perception of his angina as phantom limb pain. We feel that a good descriptive term for this phenomenon would be “phantom angina,” an exertional pain or discomfort due to coronary insufficiency appearing to occur in an already amputated upper
American
test monitor
leads
V, and aVF at rest,
December 1988 Heart Journal
at peak
extremity. In this patient, the absence of the left upper extremity and the existence of phantom limb sensation prior to the development of “phantom angina” probably delayed the appropriate diagnosis. In patients with exertional phantom limb discomfort, the possibility of “phantom angina” should be considered. REFERENCES
1. Heberden W. Some account of a disorder of the breast. Med Trans Coll Physicians (Land) 1772;2:59. 2. Rhone GF. De sensuum mendaciis a pud eos homines, quibus membrum aliquod amputatum est. Thesis. 1842; Halle. 3. Mitchell SW.- Injuries of nerves and their consequences. Philadelphia: J.B. Lippincott Co, 1872. 4. Deenadayalan CV. Anginal pain in a phantom limb (Letter). Br Med J, 1976;2:238. 5. White JC. Anatomic pathways and physiologic mechanisms. Circulation 1957;16:644. 6. Ruth TC. Pathophysiology of pain. In: Fulton JF, editor. A textbook of physiology. Philadelphia: W.B. Saunders Co, 1955:358.
Variant angina provoked by isoproterenol: An unusual cause of syncope Steven E. Jones, MD, and Andrew Birmingham, Ala.
E. Epstein,
MD.
First described by Prinzmetal et al.’ in 1959, variant angina occurs in patients with and without coronary From the University
Division of Cardiovascular of Alabama at Birmingham.
Reprint requests: sity Station-THT ham, AL 35294.
Disease,
Department
of Medicine,
Andrew E. Epstein, M.D, Division of Cardiology, 321, University of Alabama at Birmingham,
UniverBirming-
116 6, Part 1
Brief
approach. A 5F wedge balloon catheter was advanced through the aortic valve into the right ventricle. The balloon was then inflated and the catheter was easily passed across the ventricular septal defect into the pulmonary artery. Case No. 3. (Fig. 2). A 2% -year-old girl had levotransposition of the great vessels, a double-inlet single left ventricle, subaortic outflow chamber, and valvular and subvalvular pulmonary stenosis. She had previously undergone a polytetrafluoroethylene interposition graft from the left subclavian artery to the pulmonary artery. Catheterization was performed 2 years after the shunt procedure to assess her pulmonary pressures and future Fontan procedure candidacy. Her previous anatomic findings were confirmed. The venous catheter could be advanced to the atrium and then to the ventricle, but it could not be advanced further into the pulmonary artery. This difficulty was encountered because of an interrupted inferior vena cava and hemiazygous venous continuation to the high right atrium. Thus a 5F Berman catheter was advanced via the aorta to the subaortic outflow chamber, across the bulboventricular foramen into the left ventricle to the subpulmonary area and thence to the pulmonary artery. Catheter entry into the pulmonary artery is often mandatory for obtaining adequate presurgical hemodynamic and anatomic information, especially when patients have complex forms of congenital heart disease. Catheter manipulation into the pulmonary artery from the venous approach is often possible, but is sometimes difficult or impossible when patients have various forms of single ventricle anatomy or physiology, especially in conjunction with malposed great vessels and associated pulmonary stenosis. Aberrations in systemic venous anatomy, either congenital or acquired, can also interfere with adequate catheter manipulation. Lock et al.’ described this technique for use in patients with double-outlet ventricles. In this communication, the concept is expanded to include patients with single ventricular anatomy and to those with large ventricular septal defects and various forms of transposition. The method of retrograde aortic passage of a balloon catheter into the ventricle, inflation of the balloon, and usually easy pulmonary artery entry in these sit,uations allows the cardiologist to obtain the necessary rnformation for proper surgical decision making. The above case examples each demonstrated situations where obtaining hemodynamic or anatomic information was essential. We were unable to enter the pulmonary artery by conventional means in any of them, but had no problems with the retrograde aortic technique. We have found the technique simple, uncomplicated, and thus recommend its application to situations such as those described above. REFERENCE
1. Lock JE, Keane JF, Fellows KE. Diagnostic tional catheterization in congenital heart Lancaster: Martinus Nijhoff, 1987:27.
and
intervendisease. Boston,
Phantom
Communications
1627
angina
Stephen W. Mester, MD, Guillermo B. Cintron, and Charles Long, MD.” Tampa, Flu.
MD,
In the 215 years since Sir William Heberden’s original description of angina pectoris, it has been difficult to find a more eloquent description of this “disorder of the breast . . .“I Exceptions to this description of what we now know to represent myocardial ischemia have probably been noted for 214 years. A feeling of the presence of or discomfort in a limb that has been amputated has been described previously as a phantom limb sensation.‘s3 Phantom limb sensation with angina1 quality has also been reported.4 We report a case of exertional myocardial ischemia presenting as a sensation of discomfort in the phantom hand of a previously amputated left upper extremity. This 62-year-old man suffered a traumatic left upper extremity amputation at the mid-humerus in 1944. Since that time, the patient had continuously noted the “presence” of his left hand, which appeared to arise directly from his medium-length, above elbow stump. He had no discomfort until 7 years ago, when he noted a sensation of pain in his absent left hand while operating his push lawn mower. This exertional discomfort forced the patient to change to a self-propelled mower and, finally, to a riding mower. Two years ago, the patient began noting this hand pain while taking his daily walk. The pain would be reliably reproduced with walking one-half mile and would be relieved promptly with rest, and was felt to be due to his above-elbow prosthesis. The pain gradually became more frequent and severe. Multiple evaluations of his humeral stump were performed, as were a surgical revision and corticosteroid injections of the stump, without resolution of his symptoms. When a trial of walking without the prosthesis reproduced the pain, the patient was suspected of having coronary artery disease and was referred for an exercise treadmill test. The patient had a IO-year history of arterial hypertension. There was no history of hypercholesterolemia, cigarette smoking, or family history of atherosclerotic disease. Physical examination revealed a blood pressure of 145/85 mm Hg and a pulse of 76 beats/min. A well-healed left mid-humeral stump was noted, and the remainder of the examination was unremarkable. The patient underwent exercise treadmill testing. He completed 4 minutes and 26 seconds of a Bruce protocol, achieving a heart rate of 131 beats/min (81% of predicted maximal heart rate) at a blood pressure of 176/75 mm Hg. The patient experienced the typical pain in his absent left hand at 3 minutes From the Division of Cardiology and the Medicine. University of South Florida College Haley Veterans Administration Hospital. Reprint Haley
requests: VA Hospital,
‘Division of Rehabilitation of Medicine and James
S. Mester, MD, Cardiology Section (111A). 13000 Bruce B. Downs Blvd., Tampa, FL
James 33612.
A. A.
1628
Brief
Communications
Fig. 1. Computerized electrocardiographic exercise exercise, and-at 4 and 8 minutes into recovery.
into the study and subsequently developed marked ST segment depression in the inferior and lateral leads (Fig. 1). Cardiac catheterization was performed and revealed a 60% left main coronary artery stenosis, a 95% proximal left anterior descending coronary artery stenosis, a 95% first diagonal branch ostial stenosis, a 60% proximal circumflex stenosis (codominant circulation), and an 80% proximal right coronary artery stenosis. The patient underwent surgical coronary revascularization and has returned to his usual activities without recurrence of his symptoms. During repeat exercise treadmill testing, the patient completed stage 2 of a Bruce protocol, achieving a heart rate of 135 beatslmin at a blood pressure of 200175 mm Hg. The patient had no pain or electrocardiographic (ECG) changes consistent with ischemia. A sensation of “phantom limb pain” in a previously amputated limb has been reported previously. The neurologic basis for this pain is unclear; there is also an incomplete understanding of the mechanisms of angina. From the heart, afIerent nerve fibers run to the spinal cord through cardiac nerves, the upper five thoracic sympathetic ganglia, the white rami communicantes (and to a minor extent, the grey), and the upper five thoracic dorsal roots. Impulses are then transmitted through the cord to the thalamus and on to the cerebral cortex.6 In the spinal cord, some impulses mediated by the with sympathetic tierent pathway may converge impulses from somatic thoracic structures onto the same ascending spinal neurons. This may explain referred cardiac pain.6 Pain impulses may be referred to the medial aspects of the arm via common connections through the L---l . 1 &aua. UI uc*IIcu We hypothesize that these connections are a factor in this patient’s perception of his angina as phantom limb pain. We feel that a good descriptive term for this phenomenon would be “phantom angina,” an exertional pain or discomfort due to coronary insufficiency appearing to occur in an already amputated upper
American
test monitor
leads
V, and aVF at rest,
December 1988 Heart Journal
at peak
extremity. In this patient, the absence of the left upper extremity and the existence of phantom limb sensation prior to the development of “phantom angina” probably delayed the appropriate diagnosis. In patients with exertional phantom limb discomfort, the possibility of “phantom angina” should be considered. REFERENCES
1. Heberden W. Some account of a disorder of the breast. Med Trans Coll Physicians (Land) 1772;2:59. 2. Rhone GF. De sensuum mendaciis a pud eos homines, quibus membrum aliquod amputatum est. Thesis. 1842; Halle. 3. Mitchell SW.- Injuries of nerves and their consequences. Philadelphia: J.B. Lippincott Co, 1872. 4. Deenadayalan CV. Anginal pain in a phantom limb (Letter). Br Med J, 1976;2:238. 5. White JC. Anatomic pathways and physiologic mechanisms. Circulation 1957;16:644. 6. Ruth TC. Pathophysiology of pain. In: Fulton JF, editor. A textbook of physiology. Philadelphia: W.B. Saunders Co, 1955:358.
Variant angina provoked by isoproterenol: An unusual cause of syncope Steven E. Jones, MD, and Andrew Birmingham, Ala.
E. Epstein,
MD.
First described by Prinzmetal et al.’ in 1959, variant angina occurs in patients with and without coronary From the University
Division of Cardiovascular of Alabama at Birmingham.
Reprint requests: sity Station-THT ham, AL 35294.
Disease,
Department
of Medicine,
Andrew E. Epstein, M.D, Division of Cardiology, 321, University of Alabama at Birmingham,
UniverBirming-