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Small vessel phenomena in the coronary microcirculation: Phasic intramyocardial perfusion and coronary microvascular dynamics
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and bleeding, similar incidence of hemorrhage in patients receiving tissue plasminogen activator and streptokinase (fibrinogen levels lower with streptokinase), and the observation that the principal source of bleeding is the vascular access site. The second part of the article discusses the possibility of regional rather than systemic thrombolytic therapy. It also addresses the issue of laboratory monitoring of the thrombolytic state. Finally, the clinical results in deep venous thrombosis, pulmonary embolism, peripheral arterial occlusion, and myocardial infarction are indicated.
Schwartz L, Bourassa MC, Lesperance J, et al: Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty. N Engl J Med 318:1714-1719, 1988 The use of antiplatelet therapy to reduce restenosis after successful coronary angioplasty was evaluated in a randomized, double-blind, placebo-controlled study in 376 patients. Treatment consisted of oral aspirin and dipyridamole (330 mg and 75 mg) begun 24 hours before angioplasty, with the dipyridamole replaced by intravenous dipyridamole at eight hours before angioplasty. Thrombolytic therapy was resumed 16 hours after angioplasty. In addition, both groups received diltiazem, heparin, nitroglycerin, and low molecular weight dextran in the periprocedural period. Thrombolytic therapy reduced the occurrence of periprocedural transmural myocardial infarction from 13 in the placebo group to three in the treated group. However, the incidence of re-stenosis evaluated by angiography 4 to 7 months after angioplasty was similar in both treated and untreated groups (37.7% Y 38.6%).
Cohen AI, Wish MH, Fletcher RD, et al: The use and interaction of permanent pacemakers and the automatic implantable cardioverter defibrillator. Pace 11:704-711,1988 Permanent pacemakers and automatic implantable cardioverter defibrillators (AICD) may interact adversely, as indicated in this report of nine patients with both devices. Study of these patients revealed problems of AICD oversensing normal-paced rhythms, pacemaker malfunction after AICD discharge, and pacemaker undersensing of tachyarrhythmias. Oversensing of pacemaker stimuli by the AICD occurred mainly with unipolar pacemakers, necessitating exchange of unipolar for bipolar pacers in several patients. When the AICD sensed one or more pacemaker stimuli and ventricular depolarization at a rate which exceeded the rate cutoff of the AICD, the AICD discharged inappropriately. Pacemaker malfunction (inadequate sensing and capture) after AICD discharge lasted about ten seconds. Although abnormalities of pacemaker waveforms may have caused the malfunction, no waveform alterations were noted when recorded one to three minutes after AICD discharge. Another possibility is shunting of the AICD current through the pacemaker electrodes because of the zener diode in the pacemaker, which prevents current from flowing back into
CAROL L. LAKE
the pacemaker when critical voltages are exceeded. Pacemaker thresholds were unchanged after AICD discharge. Finally, pacemakers failed to sense ventricular fibrillation, and continued pacemaker stimuli inhibited discharge of the AICD. However, the pacemakers could be used for noninvasive electrophysiologic testing and induction of ventricular fibrillation in patients.
Chilian WM, Eastham CL, Layne SM, et al: Small vessel phenomena in the coronary microcirculation: Phasic intramyocardial perfusion and coronary microvascular dynamics. Prog Cardiovasc Dis 31:17-38, 1988 Most of the available information about the coronary circulation comes from measurements made on epicardial coronary arteries. This review details microvascular control mechanisms, interactions, and factors influencing flow in intramyocardial coronary arteries. The coronary circulation is characterized by a large capacitance in both epicardial and intramyocardial vasculature. Coronary venous flow continues for several seconds after cessation of coronary artery inflow, suggesting the presence of capacitance vessels. Nevertheless, diastolic flow is proportionately greater in small epicardial coronary artery and reverses during midsystole. Even in the normal myocardium, perfusion is heterogeneous and variable with the cardiac cycle. Because of active vasomotor tone, 40% to 45% of total coronary resistance is in the large microvessels. However, the concept of coronary capacitance, discussed in this review, obscures the traditional teaching of phasic intramyocardial perfusion. Another important concept discussed in this review is that of transcapillary movement of solutes in the myocardium. The capillary bed has a very large surface area with great potential for filtration of water and solutes. However, studies to date have been performed in arrested hearts (cardioplegia) that may affect the microvascular control mechanisms and tone. However, the effects of calcium-entry blockers on reperfusion injury have been studied in this model. Neither leukocytes nor platelets are requisite for the altered microvascular permeability seen in reperfusion injury. This approach may elucidate precise mechanisms of transvascular solute movement during ischemia.
Palmer DS, Nair RC, Rock G: Comparative study of the efficacy and safety of intranasal DDAVP administered to normal blood donors. Transfusion 28:311-315, 1988 DDAVP, which has achieved widespread use in cardiac patients to decrease perioperative bleeding, increases Factor VIII recovery in blood from normal donors. The findings are important since low recovery of Factor VIII by conventional techniques and insufficient supplies of donor plasma cause shortages of VIII. A double-blind comparison of the Factor VIII concentration in titrated and heparinized plasma obtained from untreated donors or donors given 300 rg of intranasal DDAVP revealed higher plasma concentrations of Factor VIII with DDAVP treatment or plasma collection in heparin. Recovery of Factor VIII in cryoprecipi-
and bleeding, similar incidence of hemorrhage in patients receiving tissue plasminogen activator and streptokinase (fibrinogen levels lower with streptokinase), and the observation that the principal source of bleeding is the vascular access site. The second part of the article discusses the possibility of regional rather than systemic thrombolytic therapy. It also addresses the issue of laboratory monitoring of the thrombolytic state. Finally, the clinical results in deep venous thrombosis, pulmonary embolism, peripheral arterial occlusion, and myocardial infarction are indicated.
Schwartz L, Bourassa MC, Lesperance J, et al: Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty. N Engl J Med 318:1714-1719, 1988 The use of antiplatelet therapy to reduce restenosis after successful coronary angioplasty was evaluated in a randomized, double-blind, placebo-controlled study in 376 patients. Treatment consisted of oral aspirin and dipyridamole (330 mg and 75 mg) begun 24 hours before angioplasty, with the dipyridamole replaced by intravenous dipyridamole at eight hours before angioplasty. Thrombolytic therapy was resumed 16 hours after angioplasty. In addition, both groups received diltiazem, heparin, nitroglycerin, and low molecular weight dextran in the periprocedural period. Thrombolytic therapy reduced the occurrence of periprocedural transmural myocardial infarction from 13 in the placebo group to three in the treated group. However, the incidence of re-stenosis evaluated by angiography 4 to 7 months after angioplasty was similar in both treated and untreated groups (37.7% Y 38.6%).
Cohen AI, Wish MH, Fletcher RD, et al: The use and interaction of permanent pacemakers and the automatic implantable cardioverter defibrillator. Pace 11:704-711,1988 Permanent pacemakers and automatic implantable cardioverter defibrillators (AICD) may interact adversely, as indicated in this report of nine patients with both devices. Study of these patients revealed problems of AICD oversensing normal-paced rhythms, pacemaker malfunction after AICD discharge, and pacemaker undersensing of tachyarrhythmias. Oversensing of pacemaker stimuli by the AICD occurred mainly with unipolar pacemakers, necessitating exchange of unipolar for bipolar pacers in several patients. When the AICD sensed one or more pacemaker stimuli and ventricular depolarization at a rate which exceeded the rate cutoff of the AICD, the AICD discharged inappropriately. Pacemaker malfunction (inadequate sensing and capture) after AICD discharge lasted about ten seconds. Although abnormalities of pacemaker waveforms may have caused the malfunction, no waveform alterations were noted when recorded one to three minutes after AICD discharge. Another possibility is shunting of the AICD current through the pacemaker electrodes because of the zener diode in the pacemaker, which prevents current from flowing back into
CAROL L. LAKE
the pacemaker when critical voltages are exceeded. Pacemaker thresholds were unchanged after AICD discharge. Finally, pacemakers failed to sense ventricular fibrillation, and continued pacemaker stimuli inhibited discharge of the AICD. However, the pacemakers could be used for noninvasive electrophysiologic testing and induction of ventricular fibrillation in patients.
Chilian WM, Eastham CL, Layne SM, et al: Small vessel phenomena in the coronary microcirculation: Phasic intramyocardial perfusion and coronary microvascular dynamics. Prog Cardiovasc Dis 31:17-38, 1988 Most of the available information about the coronary circulation comes from measurements made on epicardial coronary arteries. This review details microvascular control mechanisms, interactions, and factors influencing flow in intramyocardial coronary arteries. The coronary circulation is characterized by a large capacitance in both epicardial and intramyocardial vasculature. Coronary venous flow continues for several seconds after cessation of coronary artery inflow, suggesting the presence of capacitance vessels. Nevertheless, diastolic flow is proportionately greater in small epicardial coronary artery and reverses during midsystole. Even in the normal myocardium, perfusion is heterogeneous and variable with the cardiac cycle. Because of active vasomotor tone, 40% to 45% of total coronary resistance is in the large microvessels. However, the concept of coronary capacitance, discussed in this review, obscures the traditional teaching of phasic intramyocardial perfusion. Another important concept discussed in this review is that of transcapillary movement of solutes in the myocardium. The capillary bed has a very large surface area with great potential for filtration of water and solutes. However, studies to date have been performed in arrested hearts (cardioplegia) that may affect the microvascular control mechanisms and tone. However, the effects of calcium-entry blockers on reperfusion injury have been studied in this model. Neither leukocytes nor platelets are requisite for the altered microvascular permeability seen in reperfusion injury. This approach may elucidate precise mechanisms of transvascular solute movement during ischemia.
Palmer DS, Nair RC, Rock G: Comparative study of the efficacy and safety of intranasal DDAVP administered to normal blood donors. Transfusion 28:311-315, 1988 DDAVP, which has achieved widespread use in cardiac patients to decrease perioperative bleeding, increases Factor VIII recovery in blood from normal donors. The findings are important since low recovery of Factor VIII by conventional techniques and insufficient supplies of donor plasma cause shortages of VIII. A double-blind comparison of the Factor VIII concentration in titrated and heparinized plasma obtained from untreated donors or donors given 300 rg of intranasal DDAVP revealed higher plasma concentrations of Factor VIII with DDAVP treatment or plasma collection in heparin. Recovery of Factor VIII in cryoprecipi-