Myocardial perfusion/metabolism mismatch and ventricular arrhythmias in the chronic post infarction state^[*]

Summary

Aim: Ventricular arrhythmias have been shown to originate in the myocardial peri-infarct region due to irregular heterotopic conduction. Hypoperfused but viable myocardium is often localised in those areas and may be involved in the pathogenesis of arrhythmias. We tested the hypothesis that these myocardial perfusion/metabolism mismatches (MM) are significantly associated with ventricular arrhythmias in the chronic post infarction state. Patients, methods: 47 post infarction patients were included in the study. 33 suffered from ventricular arrhythmia whereas 14 did not. All patients underwent ^99mTc tetrofosmin SPECT and ¹⁸F-FDG PET. A region-of-interest(ROI)-analysis was used to assess viable myocardium based on predefined MM-criteria. Univariate analyses as well as a logistic regression model for the multivariate analysis were carried out. Results: 94% of the arrhythmic patients displayed at least one MM-segment as compared to 64% of the non-arrhythmic patients. MMsegments and arrhythmia showed a statistically significant relation (p = 0.018). The logistic regression model predicted the occurrence or absence of arrhythmia in 85% of all cases. Multivariate analysis gave consistent results, after adjusting for symptomatic chronic heart failure (CHF), aneurysms and age. Conclusion: Our results support the hypothesis that hypoperfused but viable myocardium represents an arrhythmogenic substrate and is a relevant risk factor for developing ventricular arrhythmias following myocardial infarction. Therefore, the detection of MM-segments allows the identification of patients with a higher risk for future cardiac events.

Zusammenfassung

Ziel: Ventrikuläre Arrhythmien entspringen häufig der myokardialen Peri-Infarktzone aufgrund irregulärer heterotoper Erregungsleitung. In diesen Zonen ist oft minderperfundiertes, jedoch vitales Myokard lokalisiert, das möglicherweise eine wichtige Rolle in der Arrhythmiegenese spielt. Diese Studie testet die Hypothese, dass dieses myokardiale Perfusions-/Stoffwechsel-Missverhältniss (MM) signifikant mit ventrikulären Arrhythmien im chronischen Post-Infarktstadium assoziiert ist. Patienten, Methoden: Einbezogen wurden 47 Post-Infarkt-Patienten (33 mit ventrikulärer Arrhythmie und 14 ohne). Alle Patienten wurden mit ^99mTc-Tetrofosmin-SPECT und ¹⁸F-FDG-PET untersucht. Anhand definierter MM-Kriterien wurde vitales Myokard mittels einer Region-of-interest(ROI)-Analyse identifiziert. Die statistische Auswertung erfolgte mittels univariater Analyse und logistischer Regression zur multivariaten Analyse. Ergebnisse: 94% der Arrhythmie-Patienten wiesen mindestens ein MM-Segment auf, im Gegensatz zu 64% der Arrhythmie-freien Patienten. Zwischen MM-Segmenten und dem Auftreten von Arrhythmien zeigte sich eine statistisch signifikante Beziehung (p = 0,018). Das logistische Regressionsmodell konnte eine Arrhythmie in 85% der Fälle voraussagen. Die multivariate Analyse führte nach Anpassung für chronische Herzinsuffizienz (CHF), Aneurysmata und Alter zu übereinstimmenden Ergebnissen. Schlussfolgerungen: Die Ergebnisse stützen die Hypothese, dass minderperfundiertes, jedoch vitales Myokard ein arrhythmogenes Substrat darstellt und ein relevanter Risikofaktor für die Entstehung ventrikulärer Arrhythmien im Post-Infarktstadium ist. Die Erkennung von MM-Segmenten ermöglicht die Identifikation von Patienten mit einem höheren Risiko für kardiale Ereignisse.

Keywords

Viable myocardium - ventricular arrhythmias - post infarction state - ^99mTc tetrofosmin SPECT - ¹⁸F-FDG PET

Schlüsselwörter

Vitales Myokard - ventrikuläre Arrhythmien - Post-Infarktstadium - ^99mTc-Tetrofosmin-SPECT - ¹⁸F-FDG-PET

• References

• 1 Altehoefer C, Kaiser HJ, Dörr R. et al. Fluorine-18 deoxyglucose PET for assessment of viable myocardium in perfusion defects in 99mTc-MIBI SPET: a comparative study in patients with coronary artery disease. Eur J Nucl Med 1992; 19: 334-42.
• 2 Altehoefer C, vom Dahl J, Biedermann M. et al. Significance of defect severity in technetium- 99m-MIBI SPECT at rest to assess myocardial viability: comparison with fluorine- 18-FDG PET. J Nucl Med 1994; 35: 569-74.
• 3 Berman DS, Kiat H, Friedman JD. et al. Separate acquisition rest thallium-201/stress technetium- 99m sestamibi dual-isotope myocardial perfusion single-photon emission computed tomography: a clinical validation study. J Am Coll Cardiol 1993; 22: 1455-64.
• 4 Breithardt G, Borggrefe M, Martinez-Rubio A. et al. Pathophysiological mechanisms of ventricular tachyarrhythmias. Eur Heart J 1989; 10 Suppl E 9-18.
• 5 Brunken R, Tillisch J, Schwaiger M. et al. Regional perfusion, glucose metabolism, and wall motion in patients with chronic electrocardiographic Q wave infarctions: evidence for persistence of viable tissue in some infarct regions by positron emission tomography. Circulation 1986; 73: 951-63.
• 6 Büll U, Foroutan Y, Hellwig D. et al. Comparison of relative ¹⁸FDG uptake with metabolic rate (MRGlucose) in the myocardium in CAD, classified by 99m-Tc-MIBI [in German]. Nuklearmedizin 1995; 34: 223-8.
• 7 Cleland JG, Chattopadhyay S, Khand A. et al. Prevalence and incidence of arrhythmias and sudden death in heart failure. Heart Fail Rev 2002; 7: 229-42.
• 8 Cobb LA, Weaver WD. Exercise: a risk for sudden death in patients with coronary heart disease. J Am Coll Cardiol 1986; 7: 215-9.
• 9 Cohen M, Wiener I, Pichard A. et al. Determinants of Ventricular-Tachycardia in Patients with Coronary- Artery Disease and Ventricular Aneurysm – Clinical, Hemodynamic, and Angiographic Factors. American Journal of Cardiology 1983; 51: 61-4.
• 10 de Bakker JM, van Capelle FJ, Janse MJ. et al. Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation. Circulation 1988; 77: 589-606.
• 11 Di Carli MF, Davidson M, Little R. et al. Value of metabolic imaging with positron emission tomography for evaluating prognosis in patients with coronary artery disease and left ventricular dysfunction. Am J Cardiol 1994; 73: 527-33.
• 12 Dillon SM, Allessie MA, Ursell PC. et al. Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ Res 1988; 63: 182-206.
• 13 Doherty JU, Kienzle MG, Waxman HL. et al. Relation of mode of induction and cycle length of ventricular tachycardia: analysis of 104 patients. Am J Cardiol 1983; 52: 60-4.
• 14 Gioia G, Bagheri B, Gottlieb CD. et al. Prediction of outcome of patients with life-threatening ventricular arrhythmias treated with automatic implantable cardioverter-defibrillators using SPECT perfusion imaging. Circulation 1997; 95: 390-4.
• 15 Gorlin R, Klein MD, Sullivan JM. Prospective Correlative Study of Ventricular Aneurysm- Mechanistic Concept and Clinical Recognition. American Journal of Medicine 1967; 42: 512-&.
• 16 Janse MJ, Vermeulen JT, Opthof T. et al. Arrhythmogenesis in heart failure. J Cardiovasc Electrophysiol 2001; 12: 496-9.
• 17 Janse MJ, Wit AL. Electrophysiological mechanisms of ventricular arrhythmias resulting from myocardial ischemia and infarction. Physiol Rev 1989; 69: 1049-169.
• 18 Jelinek MV, Lohrbauer L, Lown B. Antiarrhythmic drug therapy for sporadic ventricular ectopic arrhythmias. Circulation 1974; 49: 659-66.
• 19 Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity. A mechanism of recurrent ventricular tachycardia. Circulation 1978; 57: 659-65.
• 20 Josephson ME, Horowitz LN, Farshidi A. et al. Recurrent Sustained Ventricular Tachycardia .1. Mechanisms. Circulation 1978; 57: 431-40.
• 21 Josephson ME, Horowitz LN, Farshidi A. et al. Recurrent Sustained Ventricular Tachycardia .2. Endocardial Mapping. Circulation 1978; 57: 440-7.
• 22 Josephson RA, Papa LA, Brooks MM. et al. Effect of age on postmyocardial infarction ventricular arrhythmias (Holter Registry data from CAST I and CAST II). Cardiovascular Arrhythmia Suppression Trials. Am J Cardiol 1995; 76: 710-3.
• 23 Kannel WB, Plehn JF, Cupples LA. Cardiac-Failure and Sudden-Death in the Framingham-Study. American Heart Journal 1988; 115: 869-75.
• 24 Kempf Jr FC, Josephson ME. Cardiac arrest recorded on ambulatory electrocardiograms. Am J Cardiol 1984; 53: 1577-82.
• 25 Koch KC, vom Dahl J, Wenderdel M. et al. Myocardial viability assessment by endocardial electroanatomic mapping: comparison with metabolic imaging and functional recovery after coronary revascularization. J Am Coll Cardiol 2001; 38: 91-8.
• 26 Margolis JR, Hirshfeld Jr JW, McNeer JF. et al. Sudden death due to coronary artery disease. A clinical, hemodynamic, and angiographic profile. Circulation 1975; 52: III180-III188.
• 27 Margonato A, Bonetti F, Mailhac A. et al. Intravenous nitroglycerin suppresses exercise-induced arrhythmias in patients with ischaemic heart disease: implications for long-term treatment. Eur Heart J 1991; 12: 1278-82.
• 28 Margonato A, Mailhac A, Bonetti F. et al. Exercise- induced ischemic arrhythmias in patients with previous myocardial infarction: role of perfusion and tissue viability. J Am Coll Cardiol 1996; 27: 593-8.
• 29 Matsunari I, Fujino S, Taki J. et al. Myocardial viability assessment with technetium-99mtetrofosmin and thallium-201 reinjection in coronary artery disease. J Nucl Med 1995; 36: 1961-7.
• 30 Molajo AO, Summers GD, Bennett DH. Effect of percutaneous transluminal coronary angioplasty on arrhythmias complicating angina. Br Heart J 1985; 54: 375-7.
• 31 Moss AJ, Zareba W, Hall WJ. et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. New England Journal of Medicine 2002; 346: 877-83.
• 32 Packer M. Lack of Relation Between Ventricular Arrhythmias and Sudden-Death in Patients with Chronic Heart-Failure. Circulation 1992; 85: 50-6.
• 33 Podrid PJ, Fogel RI, Fuchs TT. Ventricular arrhythmia in congestive heart failure. Am J Cardiol 1992; 69: 82G-95G.
• 34 Rasmussen K, Lunde PI, Lie M. Coronary bypass surgery in exercise-induced ventricular tachycardia. Eur Heart J 1987; 8: 444-8.
• 35 Reiter MJ. Effects of mechano-electrical feedback: Potential arrhythmogenic influence in patients with congestive heart failure. Cardiovascular Research 1996; 32: 44-51.
• 36 Schelbert HR. Metabolic imaging to assess myocardial viability. J Nucl Med 1994; 35: 8S-14S.
• 37 Schwaiger M, Hicks R. The clinical role of metabolic imaging of the heart by positron emission tomography. J Nucl Med 1991; 32: 565-78.
• 38 vom Dahl J, Altehoefer C, Sheehan FH. et al. Effect of myocardial viability assessed by technetium- 99m-sestamibi SPECT and fluorine- 18-FDG PET on clinical outcome in coronary artery disease. J Nucl Med 1997; 38: 742-8.
• 39 vom Dahl J, Altehöfer C, Buchin P. et al. Effect of myocardial viability and coronary revascularization on clinical outcome and prognosis: a followup study of 161 patients with coronary heart disease. Z Kardiol 1996; 85: 868-81.
• 40 Weiss JN, Nademanee K, Stevenson WG. et al. Ventricular arrhythmias in ischemic heart disease. Ann Intern Med 1991; 114: 784-97.