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Acute Myocardial Infarction Associated with Intravenous Injection of Pentazocine and Tripelennamine
ing IL-1 18• 19 enters the thermoregulatory centers ofthe brain, infectious fever is believed to be due to the peripheral production ofPGE 2 , which circulates centrally to act on the hypothalamus. 20 We are unaware of any data suggesting a peripheral pyretic action of endogenous pyrogens; however, the fact that quadriplegic patients have febrile episodes at all in response to sepsis indicates that a peripheral pyretic action may be the source. Cimetidine has been described as causing fever, probably through a blockade of the H 2 receptors in the hypothalamus. 21 Ranitidine, which this patient was receiving, may also have this effect. This episode may represent a manifestation of NMS since hyperpyrexia and hemodynamic instability followed the administration of haloperidol by 12 h. Core features ofNMS are pyrexia, altered consciousness, muscular rigidity, and autonomic dysfunction progressing over 24 to 72 h. 22 The therapeutic action of neuroleptic drugs is believed to be through dopamine-receptor blockade in the basal ganglia and the hypothalamus; this central action is also believed by some to be the cause ofNMS, a hypothesis that is supported by the occurrence in patients receiving dopamine-depleting drugs. 2 A peripheral skeletal muscle mechanism similar to that seen with malignant hyperthermia has also been suggested, 3 with support being provided by skeletal muscle pathology from victims demonstrating evidence of a toxic myopathy with absent muscular glycogen and lipid stores. 4.5 In addition, dantrolene sodium, which acts peripherally on the contractile system of muscles, may be effective in some cases ofNMS,6 and muscle contracture has been induced in vitro by another neuroleptic, chlorpromazine;7 however, muscle biopsy specimens from patients surviving episodes of NMS do not appear to give abnormal in vitro halothanecaffeine contracture tests. 1 The argument for a haloperidol alone causing the hyperthermic episode is weakened by the record ofa temperature of at least 41.2°C during the 24 h prior to the administration of haloperidol; because this episode was not accompanied by hemodynamic instability, it is likely that it was a continuation of his febrile course and not another hyperpyrexic event. REFERENCES 1 Adnet PJ, Krivosie-Horber RM, Adamantidis MM, Haudecoeur G, Adnet-Bonte CA, Saulnier F, et ale The association between the neuroleptic syndrome and malignant hyperthennia. Acta Anaesthesiol Scand 1989; 33:676-80 2 Burke RE, Fahn S, Mayeux R, Weinberg H, Louis K, Willner JH. Neuroleptic malignant syndrome caused by dopamine depleting drugs in a patient with Huntington disease. Neurology (NY) 1981; 31:1022-26 3 Denborough MA, Collins S~ Hopkinson KC. Rhabdomyolysis and malignant hyperpyrexia. Br Med J (Clin Res) 1984; 1:187884 4 Martin DT, Swash M. Muscle pathology in the neuroleptic malignant syndrome. J Neuroll987; 235:120-21 5 Jones EM, Dawson A. Neuroleptic malignant syndrome: a case report with post-mortem brain and muscle pathology. J Neurol Neurosurg Psychiatry 1989; 52:1006-09 6 Guze BH, Baxter LR. Neuroleptic malignant syndrome. N Engl J Med 1985; 313:163-66 7 Andersson K. Effects of chlorpromazine, imipramine and quinidine on the mechanical activity of single skeletal muscle fibers of the frog. Acta Physiol Scand 1972; 85:532-46
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8 Bruck K, Ziesberger E. Adaptive changes in thennoregulation and their neuropharmacological basis. Pharmacol Ther 1987; 35:163-215 9 Sugarman B, Brown D, Musher D. Fever and infection in spinal cord injury patients. JAMA 1982; 248:66-70 10 Gronert GA. Malignant hyperthennia. Anesthesiology 1980; 53:395-423 11 Simon E, Pierau F-K, Taylor DCM. Central and peripheral thennal control of effectors in homeothennic temperature regulation. Physiol Rev 1986; 66:235-300 12 Simon E. Temperature regulation: the spinal cord as a site of extrahypothalamic thennoregulatory functions. Rev Physiol Biochern Pharmaco11974; 71:1-76 13 Randall WC, Rawson RO, McCook RD, Peiss CN. Central and peripheral factors in dynamic thermoregulation. J Appl Physiol 1963; 18:61-4 14 Downey JA. The spinal patient and thennoregulation. In: Hales JRS, ed. Thermal Physiology. New York: Raven Press, 1984:22528 15 Chambers ~ Seigel MS, Liu JC, Liu CN. Thennoregulatory responses of decerebrate and spinal cats. Exp Neurol 1974; 42:282-99 16 Simpson RK, Fischer OK, Ehni BL. Neurogenic hyperthermia in subarachnoid hemorrhage. South Med J 1989; 82:1577-78 17 Dascombe MJ, Milton AS. Study on the possible entry of endotoxin and prostaglandin E1 into the central nervous system from the blood. Br J Pharmaco11979; 66:565-72 18 Dinarello CA, Weiner ~ WoltJSM. Radiolabeling and disposition in rabbits of purified human leukocytic pyrogen. Clin Res 1978; 26:522A 19 Blatteis CM, Dinarello CA, Shibata M, LLanos-Q J, Quan N, Busija OW Does circulating interleukin-l enter the brain? In: Mercer JB, ed. Thermal Physiology 1989. Amsterdam: Elsevier Science Publishers, 1989:385-90 20 Milton AS. Endogenous pyrogen initiates fever by a peripheral and not a central action. In: Mercer JB, ed. Thennal Physiology 1989. Amsterdam: Elsevier Science Publishers, 1989:377-83 21 Nistico G, Rotiroti D, OeSarri A, et a1. Mechanism ofcimetidine induced fever. Lancet 1978; 2:265-66 22 Smego RA, Durack OT. The neuroleptic malignant syndrome. Arch Intern Med 1982; 142:1183-85
Acute Myocardial Infarction Associated with Intravenous Injection of Pentazocine and Tripelennamine* Bryan W MeGwier', M.D.; Martin A. Alpert, M.D., F.C.C.R; Hercules Panayiotou, M.D.; and Charles R. Lambert, M.D., Ph.D.
This case report describes the evolution of an acute anteroseptal myocardial infarction in a 27-year-old man following intravenous injection of pentazocine and tripelennamine. Subsequent coronary angiography showed normal coronary arteries. Based on the known mechanism of action of these drugs, it is postulated that myocardial infarction resulted from coronary artery spasm secondary to excessive catecholamine stimulation. (Chat 1992; 101:1730-32) *From the Division of Cardiology, University of South Alabama College of Medicine, Mobile. Reprint requests: Dr. Alpert, Division of Cardiology, 4th floor, Mastin Bldg, Suite H, Mobile, Alabama 36617 Acute Myocardial Infarction, IV Pentazocine and Tripelennamine (McGwler at 81)
drugs such as cocaine have been implicated as a I llicit cause of acute myocardial infarction. In this report, we I
describe a young man who developed acute myocardial infarction shortly after intravenous injection of pentazocine and tripelennamine. CASE REpORT
A 27-year-old black man presented to the University of South Alabama Medical Center with a complaint of crushing substernal chest pain of I-h duration. The chest pain started IS to 30 min after injection of approximately 2 to 3 ml of a mixture of 150 mg of pentazocine and 50 mg of tripelennamine dissolved in tap water and filtered through cotton. The patient was a known drug abuser, having previously used intravenous heroin and having injected pentazocine and tripelennamine intravenously on several occasions. He had no history of cardiovascular disease and had never developed chest pain following intravenous drug injection. His blood pressure on admission was 80160 mm Hg, and his pulse rate was no beats per minute. The respiratory rate and body temperature were normal. Findings from the remainder of the physical examination were normal except for the presence of needle tracks on both forearms. The resting I2-lead electrocardiogram obtained on admission showed ST-segment depression in leads VI to V•. The complete blood cell count, urinalysis, serum electrolyte levels, and chest x-ray film obtained on admission were normal. This patient's blood pressure and heart rate rapidly normalized following intravenous infusion of I L of physiologic saline solution. Chest pain continued despite normalization of blood pressure and heart rate, but rapidly abated follOwing intravenous infusion of nitroglycerin at a rate of 75 ILglkw'min. Beta-adrenergic blocking agents and morphine were not used. Following resolution of chest pain, 20 mg of nifedipine was administered orally every 6 h, and intravenous nitroglycerin was discontinued. There were no further episodes of chest pain during the hospitalization. Follow-up electrocardiograms showed evolution of an acute Qwave anteroseptal myocardial infarction with associated lateral ischemia. The total serum creatine kinase level rose to a peak of 2,840 IV at 24 h, with an MB fraction of 14 percent. Toxicologic evaluation of whole blood tested positive for pentazocine and tripelennamine but negative for cocaine, opiates, and other commonly abused drugs. Diagnostic left heart catheterization and coronary angiography performed 7 days after the event showed mild anterolateral hypokinesia, a left ventricular ejection fraction of 50 percent, and a left ventricular end-diastolic pressure of 12 mm Hg. The coronary angiogram showed normal epicardial coronary arteries (Fig IA and IB). The patients remaining course of hospitalization was uneventful. DISCUSSION
In recent years, intravenous injection of pentazocine and tripelennamine has been used increasingly by drug abusers to achieve a heroin-like euphoria.'.3 This particular combination is frequently referred to as 'IS and 8's" or 'IS and blues;' the 'I' representing the first letter of the brand name, Talwin, and the "8's" or "blues" referring to the color of tripelennamine tablets.'.3 Intravenous injection of pentazocine and tripelennamine in combination has been reported to produce nausea, vomiting, headache, seizures, agitation, anxiety, muscle spasms, syncope and presyncope, and elevation of systolic and diastolic blood pressure.2-' Chest pain has been previously described;··3 however, this is the first reported case of acute myocardial infarction associated with intravenous injection of pentazocine and tripelennamine.
FIGURE I. Coronary angiowam showin~ normal left coronary system and normal right coronary artery.
Pentazocine has both opioid agonist and weak antagonist properties. U In patients with acute myocardial infarction, it has been shown to raise systemic vascular resistance, which may relate to its ability to increase serum catecholamine levels.· Tripelennamine is a histamine receptor antagonist that also increases serum catecholamine levels. In addition, it exerts a cocaine-like effect by preventing reuptake of neurotransmitters in nerve endings. Cocaine has been shown to block reuptake of norepinephrine in the synaptic clefts of a variety of tissues, including vascular smooth muscle and myocardium. Such blockade enhances adrenergic stimulation. In long-term cocaine abusers, depletion of dopamine prevents stimulation of dopamine-l receptors, resulting in loss of the protective vasodilative effect. It is possible that pentazocine and tripelennamine might produce similar biochemical changes. Excessive adrenergic stimulation in affected individuals might lead to coronary artery spasm or excessive myocardial oxygen consumption (or both), potentially resulting in myocardial ischemia or infarction. If such is the case, then administration of ~-adrenergic blocking agents would theoretically be CHEST I 101 I 6 I JUNE. 1992
1731
contraindicated, due to resultant unopposed a-adrenergic stimulation. Administration of a-adrenergic blocking drugs (eg phentolamine), calcium-channe1 blocking agents, and possibly intravenous nitroglycerin or nitroprusside would be more rational therapeutic choices. REFERENCES
I Schneider OJ. Cardiac ramifications of cocaine abuse. Coronary Artery Dis 1991; 2:267-73 2 Polkis A, Whyatt PL. Current trends in the abuse of pentazocine and tripelennamine: the metropolitan St. Louis experience. J Forensic Sci 1988; 25:72-8 3 DeBand ML, Jagger]A. T'sand B's: midwestern heroin substitute. Clin Toxicoll98l; 18:1117-23 4 Lange WR, Lasinki DR. The clinical pharmacology ofpentazocine and tripelennamine (T's and B's). Adv Alcohol Subst Abuse 1986; 5:71-83 5 Thompson EB: Cardiovascular effects of pentazocine and tripelennamine in combination in conscious rats. Res Comm Subst Abuse 1983; 4:201-14 6 Nagle RE, Pilcher J. Respiratory and circulatory effect of pantazocine: reviewing analgesics often used in myocardial infarction. Br Heart J 1972; 34:244-51
Mitral and Tricuspid Annular Endocarditis· Diagnosis by Transesophageal Echocardlography Mohandas M. Shenoy, M.D.; and Kulandaivelu Chandrasekaran, M.D.
Two cases of infective endocarditis with vegetations attached to the mitral and tricuspid annuli are described. In
both cases, the vegetations could not be identified by transthoracic echocardiography. These cases illustrate the advantage of TEE over the transthoracic approach in recognizing vegetations in extravalvular locations.
I I
(Cheat 1992; 101:1132·33)
TEE = transesophageaI echocardiography
I
FIGURE I. Transesophageal echocardiogram showing a large vegetation (v) attached to the mitral annulus. The mitral leaflets (arrowheads) are normal. LA = left atrium; RA = right atrium. nation of the heart and lungs was normal. The chest roentgenogram and electrocardiogram were normal. There was leukocytosis with neutrophilia. Blood culture yielded a growth of W'OUp G hetahemolytic Streptncoccus. The patient was treated with intravenously administered ampicillin. Infective endocarditis wa~ suspected when a new apical systolic murmur developed. Transthoracic echocardiow-aphy was of poor quality due to the obesity of the patient (weight, 280 lb). There was no obvious eviden<.'e of ve~etation on the heart valves. A nonmoving echodensity was noted in the region of the posterior mitral annulus. In view of the typical location and appearance of this abnormality, calcification of the mitral annulus, a finding commonly seen in older patients, was dia~osed. On the tenth day, the patient developed transient aphasia and a mild left hemiparesis which led to the suspected dia~osis of cerebral embolism. A repeated echocardiowam showed no change. A TEE was performed. The lesion which was initially dia~osed as mitral annular calcification was indeed a large, shaggy vegetation attached to the mitral annulus and to the base of the posterior mitral leaflet (Fig I). The mitral annulus was minimally calcified. The patient was discharged after six weeks of antibiotic therapy. A predischarge echocardiogram showed an appreciable reduction in the size and the density ofthe mitral annular vegetation. CASE 2 A SS-yellN)ld woman presented with an acute inferior wall
nfective endocarditis is a serious disease that requires prompt recognition and treatment. Although echocardiography has vastly improved our ability to diagnose this condition rapidly, a diagnostically adequate transthoracic echocardiographic study may not always be possible. Poor quality of images may result when certain physical characteristics of the patients (such as obesity) and chest diseases (such as emphysema) impede the transmission of ultrasound. With TEE, these difficulties are circumvented. The following cases illustrate the superior diagnostic ability of TEE over the conventional, transthoracic echocardiography in detecting vegetations located in unusual sites within the heart. CASE REPORTS
CASE I A 74-year-old man was hospitalized with high fever. The exami·From the Division ofCardiology, Departments of Medicine, Coney Island Hospital, SUNY-Health Sciences Center, Brooklyn, NY.
1732
FIGURE 2. Transesophageal echocardiogram showing a vegeta~on (v) attached to the tricuspid annulus. LA = left atrium; RA=nght atrium. Mitral and Tricuspid Annular Endocarditis (Shenoy. Chandraselceran)
1730
8 Bruck K, Ziesberger E. Adaptive changes in thennoregulation and their neuropharmacological basis. Pharmacol Ther 1987; 35:163-215 9 Sugarman B, Brown D, Musher D. Fever and infection in spinal cord injury patients. JAMA 1982; 248:66-70 10 Gronert GA. Malignant hyperthennia. Anesthesiology 1980; 53:395-423 11 Simon E, Pierau F-K, Taylor DCM. Central and peripheral thennal control of effectors in homeothennic temperature regulation. Physiol Rev 1986; 66:235-300 12 Simon E. Temperature regulation: the spinal cord as a site of extrahypothalamic thennoregulatory functions. Rev Physiol Biochern Pharmaco11974; 71:1-76 13 Randall WC, Rawson RO, McCook RD, Peiss CN. Central and peripheral factors in dynamic thermoregulation. J Appl Physiol 1963; 18:61-4 14 Downey JA. The spinal patient and thennoregulation. In: Hales JRS, ed. Thermal Physiology. New York: Raven Press, 1984:22528 15 Chambers ~ Seigel MS, Liu JC, Liu CN. Thennoregulatory responses of decerebrate and spinal cats. Exp Neurol 1974; 42:282-99 16 Simpson RK, Fischer OK, Ehni BL. Neurogenic hyperthermia in subarachnoid hemorrhage. South Med J 1989; 82:1577-78 17 Dascombe MJ, Milton AS. Study on the possible entry of endotoxin and prostaglandin E1 into the central nervous system from the blood. Br J Pharmaco11979; 66:565-72 18 Dinarello CA, Weiner ~ WoltJSM. Radiolabeling and disposition in rabbits of purified human leukocytic pyrogen. Clin Res 1978; 26:522A 19 Blatteis CM, Dinarello CA, Shibata M, LLanos-Q J, Quan N, Busija OW Does circulating interleukin-l enter the brain? In: Mercer JB, ed. Thermal Physiology 1989. Amsterdam: Elsevier Science Publishers, 1989:385-90 20 Milton AS. Endogenous pyrogen initiates fever by a peripheral and not a central action. In: Mercer JB, ed. Thennal Physiology 1989. Amsterdam: Elsevier Science Publishers, 1989:377-83 21 Nistico G, Rotiroti D, OeSarri A, et a1. Mechanism ofcimetidine induced fever. Lancet 1978; 2:265-66 22 Smego RA, Durack OT. The neuroleptic malignant syndrome. Arch Intern Med 1982; 142:1183-85
Acute Myocardial Infarction Associated with Intravenous Injection of Pentazocine and Tripelennamine* Bryan W MeGwier', M.D.; Martin A. Alpert, M.D., F.C.C.R; Hercules Panayiotou, M.D.; and Charles R. Lambert, M.D., Ph.D.
This case report describes the evolution of an acute anteroseptal myocardial infarction in a 27-year-old man following intravenous injection of pentazocine and tripelennamine. Subsequent coronary angiography showed normal coronary arteries. Based on the known mechanism of action of these drugs, it is postulated that myocardial infarction resulted from coronary artery spasm secondary to excessive catecholamine stimulation. (Chat 1992; 101:1730-32) *From the Division of Cardiology, University of South Alabama College of Medicine, Mobile. Reprint requests: Dr. Alpert, Division of Cardiology, 4th floor, Mastin Bldg, Suite H, Mobile, Alabama 36617 Acute Myocardial Infarction, IV Pentazocine and Tripelennamine (McGwler at 81)
drugs such as cocaine have been implicated as a I llicit cause of acute myocardial infarction. In this report, we I
describe a young man who developed acute myocardial infarction shortly after intravenous injection of pentazocine and tripelennamine. CASE REpORT
A 27-year-old black man presented to the University of South Alabama Medical Center with a complaint of crushing substernal chest pain of I-h duration. The chest pain started IS to 30 min after injection of approximately 2 to 3 ml of a mixture of 150 mg of pentazocine and 50 mg of tripelennamine dissolved in tap water and filtered through cotton. The patient was a known drug abuser, having previously used intravenous heroin and having injected pentazocine and tripelennamine intravenously on several occasions. He had no history of cardiovascular disease and had never developed chest pain following intravenous drug injection. His blood pressure on admission was 80160 mm Hg, and his pulse rate was no beats per minute. The respiratory rate and body temperature were normal. Findings from the remainder of the physical examination were normal except for the presence of needle tracks on both forearms. The resting I2-lead electrocardiogram obtained on admission showed ST-segment depression in leads VI to V•. The complete blood cell count, urinalysis, serum electrolyte levels, and chest x-ray film obtained on admission were normal. This patient's blood pressure and heart rate rapidly normalized following intravenous infusion of I L of physiologic saline solution. Chest pain continued despite normalization of blood pressure and heart rate, but rapidly abated follOwing intravenous infusion of nitroglycerin at a rate of 75 ILglkw'min. Beta-adrenergic blocking agents and morphine were not used. Following resolution of chest pain, 20 mg of nifedipine was administered orally every 6 h, and intravenous nitroglycerin was discontinued. There were no further episodes of chest pain during the hospitalization. Follow-up electrocardiograms showed evolution of an acute Qwave anteroseptal myocardial infarction with associated lateral ischemia. The total serum creatine kinase level rose to a peak of 2,840 IV at 24 h, with an MB fraction of 14 percent. Toxicologic evaluation of whole blood tested positive for pentazocine and tripelennamine but negative for cocaine, opiates, and other commonly abused drugs. Diagnostic left heart catheterization and coronary angiography performed 7 days after the event showed mild anterolateral hypokinesia, a left ventricular ejection fraction of 50 percent, and a left ventricular end-diastolic pressure of 12 mm Hg. The coronary angiogram showed normal epicardial coronary arteries (Fig IA and IB). The patients remaining course of hospitalization was uneventful. DISCUSSION
In recent years, intravenous injection of pentazocine and tripelennamine has been used increasingly by drug abusers to achieve a heroin-like euphoria.'.3 This particular combination is frequently referred to as 'IS and 8's" or 'IS and blues;' the 'I' representing the first letter of the brand name, Talwin, and the "8's" or "blues" referring to the color of tripelennamine tablets.'.3 Intravenous injection of pentazocine and tripelennamine in combination has been reported to produce nausea, vomiting, headache, seizures, agitation, anxiety, muscle spasms, syncope and presyncope, and elevation of systolic and diastolic blood pressure.2-' Chest pain has been previously described;··3 however, this is the first reported case of acute myocardial infarction associated with intravenous injection of pentazocine and tripelennamine.
FIGURE I. Coronary angiowam showin~ normal left coronary system and normal right coronary artery.
Pentazocine has both opioid agonist and weak antagonist properties. U In patients with acute myocardial infarction, it has been shown to raise systemic vascular resistance, which may relate to its ability to increase serum catecholamine levels.· Tripelennamine is a histamine receptor antagonist that also increases serum catecholamine levels. In addition, it exerts a cocaine-like effect by preventing reuptake of neurotransmitters in nerve endings. Cocaine has been shown to block reuptake of norepinephrine in the synaptic clefts of a variety of tissues, including vascular smooth muscle and myocardium. Such blockade enhances adrenergic stimulation. In long-term cocaine abusers, depletion of dopamine prevents stimulation of dopamine-l receptors, resulting in loss of the protective vasodilative effect. It is possible that pentazocine and tripelennamine might produce similar biochemical changes. Excessive adrenergic stimulation in affected individuals might lead to coronary artery spasm or excessive myocardial oxygen consumption (or both), potentially resulting in myocardial ischemia or infarction. If such is the case, then administration of ~-adrenergic blocking agents would theoretically be CHEST I 101 I 6 I JUNE. 1992
1731
contraindicated, due to resultant unopposed a-adrenergic stimulation. Administration of a-adrenergic blocking drugs (eg phentolamine), calcium-channe1 blocking agents, and possibly intravenous nitroglycerin or nitroprusside would be more rational therapeutic choices. REFERENCES
I Schneider OJ. Cardiac ramifications of cocaine abuse. Coronary Artery Dis 1991; 2:267-73 2 Polkis A, Whyatt PL. Current trends in the abuse of pentazocine and tripelennamine: the metropolitan St. Louis experience. J Forensic Sci 1988; 25:72-8 3 DeBand ML, Jagger]A. T'sand B's: midwestern heroin substitute. Clin Toxicoll98l; 18:1117-23 4 Lange WR, Lasinki DR. The clinical pharmacology ofpentazocine and tripelennamine (T's and B's). Adv Alcohol Subst Abuse 1986; 5:71-83 5 Thompson EB: Cardiovascular effects of pentazocine and tripelennamine in combination in conscious rats. Res Comm Subst Abuse 1983; 4:201-14 6 Nagle RE, Pilcher J. Respiratory and circulatory effect of pantazocine: reviewing analgesics often used in myocardial infarction. Br Heart J 1972; 34:244-51
Mitral and Tricuspid Annular Endocarditis· Diagnosis by Transesophageal Echocardlography Mohandas M. Shenoy, M.D.; and Kulandaivelu Chandrasekaran, M.D.
Two cases of infective endocarditis with vegetations attached to the mitral and tricuspid annuli are described. In
both cases, the vegetations could not be identified by transthoracic echocardiography. These cases illustrate the advantage of TEE over the transthoracic approach in recognizing vegetations in extravalvular locations.
I I
(Cheat 1992; 101:1132·33)
TEE = transesophageaI echocardiography
I
FIGURE I. Transesophageal echocardiogram showing a large vegetation (v) attached to the mitral annulus. The mitral leaflets (arrowheads) are normal. LA = left atrium; RA = right atrium. nation of the heart and lungs was normal. The chest roentgenogram and electrocardiogram were normal. There was leukocytosis with neutrophilia. Blood culture yielded a growth of W'OUp G hetahemolytic Streptncoccus. The patient was treated with intravenously administered ampicillin. Infective endocarditis wa~ suspected when a new apical systolic murmur developed. Transthoracic echocardiow-aphy was of poor quality due to the obesity of the patient (weight, 280 lb). There was no obvious eviden<.'e of ve~etation on the heart valves. A nonmoving echodensity was noted in the region of the posterior mitral annulus. In view of the typical location and appearance of this abnormality, calcification of the mitral annulus, a finding commonly seen in older patients, was dia~osed. On the tenth day, the patient developed transient aphasia and a mild left hemiparesis which led to the suspected dia~osis of cerebral embolism. A repeated echocardiowam showed no change. A TEE was performed. The lesion which was initially dia~osed as mitral annular calcification was indeed a large, shaggy vegetation attached to the mitral annulus and to the base of the posterior mitral leaflet (Fig I). The mitral annulus was minimally calcified. The patient was discharged after six weeks of antibiotic therapy. A predischarge echocardiogram showed an appreciable reduction in the size and the density ofthe mitral annular vegetation. CASE 2 A SS-yellN)ld woman presented with an acute inferior wall
nfective endocarditis is a serious disease that requires prompt recognition and treatment. Although echocardiography has vastly improved our ability to diagnose this condition rapidly, a diagnostically adequate transthoracic echocardiographic study may not always be possible. Poor quality of images may result when certain physical characteristics of the patients (such as obesity) and chest diseases (such as emphysema) impede the transmission of ultrasound. With TEE, these difficulties are circumvented. The following cases illustrate the superior diagnostic ability of TEE over the conventional, transthoracic echocardiography in detecting vegetations located in unusual sites within the heart. CASE REPORTS
CASE I A 74-year-old man was hospitalized with high fever. The exami·From the Division ofCardiology, Departments of Medicine, Coney Island Hospital, SUNY-Health Sciences Center, Brooklyn, NY.
1732
FIGURE 2. Transesophageal echocardiogram showing a vegeta~on (v) attached to the tricuspid annulus. LA = left atrium; RA=nght atrium. Mitral and Tricuspid Annular Endocarditis (Shenoy. Chandraselceran)