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Angina and exertional myocardial ischemia in diabetic and nondiabetic patients: Assessment by exercise thallium scintigraphy
LITERATURE REVIEW
Local cerebral blood flow (ICBF) decreased 19% after 25 days and 25% after 70 days of potassium depletion in 30 of 31 cerebral structures. Local cerebral glucose use was unchanged at either time, although it was measured in different animals than ICBF. There was a strong positive correlation between cerebral blood flow and glucose use during potassium depletion. Cisternal cerebrospinal fluid (CSF) potassium concentration decreased while pH and PC02 increased. Strong anion difference in the CSF increased, secondary to an increased bicarbonate, chloride ion was reduced, and sodium was unchanged. In muscle, the loss of potassium was compensated by a gain in sodium. The increase in CSF PC4 results from decreased CBF.
Nesto RW, Phillips RT, Keb KG, et al: Angina and exertional myocardial ischemia in diabetic and nondiabetic patients: Assessment by exercise thallium scintigraphy. Ann Intern Med 108:170-175,1988 Diabetic neuropathy affects cardiac afferent sensory fibers, interfering with pain transmission. Thus, diabetic patients are at risk for severe ischemia without the early warning of angina. This study of 100 consecutive patients, 50 diabetic patients (defined as hyperglycemia requiring oral hypoglycemic drugs or insulin), and 50 nondiabetic patients undergoing exercise tolerance tests demonstrated angina in 14 of 50 diabetic patients as compared to 34 of 50 nondiabetic patients (P < .OOOl). The two groups were similar with respect to type or number of antianginal medications, indications for exercise testing, and reasons for test termination. Hypertension was more common in the diabetic group. Although the results appear conclusive, the reason for physician ordering of an exercise test could have biased the results. In diabetic patients, periodic evaluation for myocardial ischemia by exercise testing may provide valuable assessment of the severity of coronary disease when angina is absent or unchanged.
Mackenzie JE, Frank LW: Inlhtence of pretreatment with a monoamine oxidase inhibitor iphenelzine) on the effects of buprenorphine and pethidine in the conscious rat. Br J Anaesth 60~216221,1988 Buprenorphine, an opioid partial agonist, was tested in rabbits for possible interactions with the monoamine oxidase inhibitor (MAOI) phenelzine. As compared with saline or meperidine, buprenorphine, 0.1 or 1 mg/kg, had minimal or no effect on behavior, body temperature, heart rate, or blood pressure. Meperidine, given after phenelzine, caused increased blood pressure and temperature, tachycardia, hyperexcitement, motor restlessness, and death in three of six animals. Thus, buprenorphine may be a safe alternative analgesic in the presence of MAOI. In the same issue of the journal, Stack et al (Br J Anaesth 60:220-227, 1988) review the potential interactions between MAO1 and drugs used in the perioperative period. With the exception of meperidine and dextromethorphan, serious or fatal interactions with narcotics are rare or
709
unknown. Although the evidence is anecdotal, the safety of fentanyl with MAO1 appears likely. The interaction of meperidine with MAO1 takes two forms: (a) an excitatory form characterized by headache, unmanageable behavior, agitation, hypotension or hypertension, progressing to hyperthermia, rigidity, convulsions, and coma attributable to central serotonergic overactivity; and (b) a depressive form caused by inhibition of hepatic microenzymes by MAO1 with accumulation of free narcotic resulting in respiratory depression, hypotension, and coma. No undesirable interactions between MAO1 and neuromuscular blockers were noted, except for decreased pseudocholinesterase levels after phenelzine and release of stored epinephrine by pancuronium, which might exaggerate an excitatory response. Other theoretical responses include worsened excitatory interactions by atropine and increased reductive metabolites of halothane. Relatively safe drugs for perioperative care of patients taking MAO1 include buprenorphine, fentanyl, morphine, isoflurane, nitrous oxide, enflurane, vecuronium, and atracurium. Continuation of MAO1 through the perioperative period is warranted to prevent compromise of the patient’s psychiatric illness, although the possibility of sympathetic overactivity is always present.
McIvor ME, Williams GM, Brinker J: Subclavian-coronary steal through a LIMA-to-LAD bypass graft. Cathet Cardiovasc Diagn 14:100104,1988 Patency of the left subclavian artery is essential to successful left internal mammary artery grafting to the coronary circulation. The authors report a single case of stenosis of the left subclavian artery at its origin that resulted in retrograde flow through the LIMA graft, causing both arm and myocardial ischemia. Correction of the subclavian stenosis with a carotid-to-subclavian bypass restored anterograde flow in the LIMA and resolved the exertional ischemia of the left arm.
Garan H, McGovern BA, CanzaneiIo VJ, et al: The effect of potassium ion depletion on postinfarction canine cardiac arrhythmias. Circulation 77~696704,1988 Like the study of Shrock and Kuschinsky reported above, this study confirms the deleterious effects of hypokalemia. The authors confirmed a significant correlation between the magnitude of cumulative potassium deficit and the likelihood of spontaneous ventricular fibrillation during experimental myocardial infarction. The protocol included animals made hypokalemic by dietary potassium deprivation with or without diuretic administration. Although hemodynamic variables did not differ among the groups, the plasma potassium at the time of coronary ligation was decreased in potassium-deprived animals. With myocardial infarction involving 14% to 22% of left ventricular mass, animals with a mean cumulative potassium deficit of -4.01 * 2.19 mEq/kg developed spontaneous ventricular fibrillation, whereas those with a deficit of only -0.11 mEq/kg did not. Cumulative potassium deficit, but not plasma potassium concentration,
Local cerebral blood flow (ICBF) decreased 19% after 25 days and 25% after 70 days of potassium depletion in 30 of 31 cerebral structures. Local cerebral glucose use was unchanged at either time, although it was measured in different animals than ICBF. There was a strong positive correlation between cerebral blood flow and glucose use during potassium depletion. Cisternal cerebrospinal fluid (CSF) potassium concentration decreased while pH and PC02 increased. Strong anion difference in the CSF increased, secondary to an increased bicarbonate, chloride ion was reduced, and sodium was unchanged. In muscle, the loss of potassium was compensated by a gain in sodium. The increase in CSF PC4 results from decreased CBF.
Nesto RW, Phillips RT, Keb KG, et al: Angina and exertional myocardial ischemia in diabetic and nondiabetic patients: Assessment by exercise thallium scintigraphy. Ann Intern Med 108:170-175,1988 Diabetic neuropathy affects cardiac afferent sensory fibers, interfering with pain transmission. Thus, diabetic patients are at risk for severe ischemia without the early warning of angina. This study of 100 consecutive patients, 50 diabetic patients (defined as hyperglycemia requiring oral hypoglycemic drugs or insulin), and 50 nondiabetic patients undergoing exercise tolerance tests demonstrated angina in 14 of 50 diabetic patients as compared to 34 of 50 nondiabetic patients (P < .OOOl). The two groups were similar with respect to type or number of antianginal medications, indications for exercise testing, and reasons for test termination. Hypertension was more common in the diabetic group. Although the results appear conclusive, the reason for physician ordering of an exercise test could have biased the results. In diabetic patients, periodic evaluation for myocardial ischemia by exercise testing may provide valuable assessment of the severity of coronary disease when angina is absent or unchanged.
Mackenzie JE, Frank LW: Inlhtence of pretreatment with a monoamine oxidase inhibitor iphenelzine) on the effects of buprenorphine and pethidine in the conscious rat. Br J Anaesth 60~216221,1988 Buprenorphine, an opioid partial agonist, was tested in rabbits for possible interactions with the monoamine oxidase inhibitor (MAOI) phenelzine. As compared with saline or meperidine, buprenorphine, 0.1 or 1 mg/kg, had minimal or no effect on behavior, body temperature, heart rate, or blood pressure. Meperidine, given after phenelzine, caused increased blood pressure and temperature, tachycardia, hyperexcitement, motor restlessness, and death in three of six animals. Thus, buprenorphine may be a safe alternative analgesic in the presence of MAOI. In the same issue of the journal, Stack et al (Br J Anaesth 60:220-227, 1988) review the potential interactions between MAO1 and drugs used in the perioperative period. With the exception of meperidine and dextromethorphan, serious or fatal interactions with narcotics are rare or
709
unknown. Although the evidence is anecdotal, the safety of fentanyl with MAO1 appears likely. The interaction of meperidine with MAO1 takes two forms: (a) an excitatory form characterized by headache, unmanageable behavior, agitation, hypotension or hypertension, progressing to hyperthermia, rigidity, convulsions, and coma attributable to central serotonergic overactivity; and (b) a depressive form caused by inhibition of hepatic microenzymes by MAO1 with accumulation of free narcotic resulting in respiratory depression, hypotension, and coma. No undesirable interactions between MAO1 and neuromuscular blockers were noted, except for decreased pseudocholinesterase levels after phenelzine and release of stored epinephrine by pancuronium, which might exaggerate an excitatory response. Other theoretical responses include worsened excitatory interactions by atropine and increased reductive metabolites of halothane. Relatively safe drugs for perioperative care of patients taking MAO1 include buprenorphine, fentanyl, morphine, isoflurane, nitrous oxide, enflurane, vecuronium, and atracurium. Continuation of MAO1 through the perioperative period is warranted to prevent compromise of the patient’s psychiatric illness, although the possibility of sympathetic overactivity is always present.
McIvor ME, Williams GM, Brinker J: Subclavian-coronary steal through a LIMA-to-LAD bypass graft. Cathet Cardiovasc Diagn 14:100104,1988 Patency of the left subclavian artery is essential to successful left internal mammary artery grafting to the coronary circulation. The authors report a single case of stenosis of the left subclavian artery at its origin that resulted in retrograde flow through the LIMA graft, causing both arm and myocardial ischemia. Correction of the subclavian stenosis with a carotid-to-subclavian bypass restored anterograde flow in the LIMA and resolved the exertional ischemia of the left arm.
Garan H, McGovern BA, CanzaneiIo VJ, et al: The effect of potassium ion depletion on postinfarction canine cardiac arrhythmias. Circulation 77~696704,1988 Like the study of Shrock and Kuschinsky reported above, this study confirms the deleterious effects of hypokalemia. The authors confirmed a significant correlation between the magnitude of cumulative potassium deficit and the likelihood of spontaneous ventricular fibrillation during experimental myocardial infarction. The protocol included animals made hypokalemic by dietary potassium deprivation with or without diuretic administration. Although hemodynamic variables did not differ among the groups, the plasma potassium at the time of coronary ligation was decreased in potassium-deprived animals. With myocardial infarction involving 14% to 22% of left ventricular mass, animals with a mean cumulative potassium deficit of -4.01 * 2.19 mEq/kg developed spontaneous ventricular fibrillation, whereas those with a deficit of only -0.11 mEq/kg did not. Cumulative potassium deficit, but not plasma potassium concentration,