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Right ventricular infarction
LEllERS
in select cases of Prinxmetal’s angina suggests that spasm may be responsible for angina, myocardial infarction, and even sudden death in some patients with hypertrophic obstructive cardiomyopathy.4 The evolution of the role of spasm in hypertrophic obstructive cardiomyopathy is in parallel with its recent development as a pathogenetic mechanism causing chest pain, acute myocardial infarction and possibly sudden death in select patients with the mitral valve prolapse syndrome. Chesler et al5 reported on four patients with the billowing mitral leaflet syndrome and acute myocardial infarction who were subsequently found to have angiographically normal coronary arteries. These authors postulated coronary arterial spasm as the cause. This concept received further support from Buda et al.,6 who found 9 of 10 patients with coronary spasm to have angiographic mitral valve prolapse, although in 8 the spasm occurred at the catheter tip. However, we7 recently encountered four patients with the prolapse-click syndrome who have evidence of spontaneous or ergonovineinduced coronary spasm. Recently, it has been well documented that attacks of variant angina can result in acute myocardial infarction, even in the absence of atherosclerosis. Furthermore, pain appears to be an insensitive measure of the occurrence of coronary spasm as demonstrated by ambulatory monitoring of three patients with variant angina.9 Of 1,045 spontaneous episodes of S-T segment elevation 89 percent were totally asymptomatic. Coronary arterial vasospasm appears to be a significant clinical entity. Its best method of identification and exact contribution to various forms of cardiac disease still remains to be defined. Richard K. Mautner, MD, FACC John H. Phillips, MD, FACC Department of Cardiology Tulane University New Orleans, Louisiana References 1. Muon BJ, f!pmtohs2 Robwfa WC. Hypetlrophk cardiomyopathyand tranamlNal myoolvdtalItWctkn withoutrl@fkant athemscleronisof tha inbnnwai wlonary arterl6s. Am J Can%l1979:49:1089-1102. 2. MWb!8f WC,Than88 f, Dhurdu R, Pftfif@ Jff. F&)ertrophk dx4ructkn cardle myopathyawl ceronuy * spasm.chest, in peas. 3. @odwfn Jf. ?it+SS?fiOCM?ASH. A plea for unity.Am iia.w 1975;39:269-77. 4. fWCfDR,QldcAE.CWmoPR,Quhanuff,HanimnLlCAlkreda&wt#cactfvHy in comnwy mtay spawn. Am J Ctwdlol1979;43:1073-9. 5. ~EuYarE,~JA~af.A~~~~withnomtaicaonary art01W: a poMibk ~ifestatkn of the billowingleafiat syndrome. Clrcuiatkn 1976; 54203-g. 6. SudaYLawnaDGMyum110,~at.Cwmmywteyspe3mandmthivafueprolapse. Am lhft J 1978;95:457-62. 8. W JE. The syn&cmaof vsrbnt angfnaadmhatf~ in acue myotxdtal InfarctIon. chudatkn 1979;59:297-306. 9. RQhon4PIbnonRY.WLrAa~JA.F~OC.V~~~na: IWwkn of Wax08 of sympametk nervoussystemhnct~on.Am J Cardki 1979; 4331090-5.
RIGHT VENTRICULAR
FIGURE 1.
Right ventricular intracavitary recording.
electrocardiogram showed a definite pattern of injury (S-T segment elevations representing a current of injury with the electrode in endocardial contact; Fig. 1). In all three patients a pattern of right ventricular involvement was evident on technetium99m stannous pyrophosphate scanning. Only two of these patients presented with the hemodynamic signs that would usually arouse the suspicion of right ventricular involvement. Moreover, surface electrode recordings over the right precordium revealed no abnormality. An intracavitary electrocardiogram was also recorded in five patients with the sick sinus syndrome who had a temporary pacemaker inserted. The results were a normal intracavitary pattern with an isoelectric S-T segment. Of particular interest is a case of a patient with an extensive anterior myocardial infarction and a right bundle branch block. Intracavitary recordings, made at various sites during pacemaker electrode insertion under fluoroscopic control, showed septal and right ventricular involvement. Technetium-99m stannous pyrophosphate scans suggested only anterior myocardial infarction without hinting at the true extent of the damage. Facilities for nuclear scanning are not always at hand, whereas pacemakers are readily available. It may be useful to perform right ventricular recordings as a routine procedure in all cases in which a pacemaker is indicated. This procedure may unmask right ventricular extension of infarction even in cases in which it may not be hemodynamically obvious nor indicated on technetium-99m pyrophosphate scans. A. Marmor, MD G. Alpan A. Palant, MD Department of Cardiology Carmel Hospital Haifa, Israel
INFARCTION
There has been renewed interest in right ventricular infarction.‘p2 It is clear that a major difficulty lies in the antemortem diagnosis. We wish to report a simple and readily available method that may aid such diagnosis. In six patients with inferior wall myocardial infarction, the appearance of A-V block required the insertion of a temporary pacemaker. Before the electrode was connected to the pulse generator, an intracavitary recording was made by connecting the distal pole of the pacemaker electrode to the chest lead electrode of the electrocardiographic recorder. In three patients the intracavitary
TO THE EDITOR
References 1. bmrJM,Rofmi#WC.Ri@evecrlrlcular intarctknwmpiicatmgleftvelwicularinfarctkn Secondaryto cwonary heart disease. Am J Cardioi1978;42:985-94. 2. f_cetl I), Lof&adl RC. pohal GM, * al. Ri9htventrkxdarInfwctioo.Clinicaldia9noak and differentlatlonfrom cardiactamponadeand pwkardlal oons!xictlon. Am J Cardiol 1979;43:465-71.
Auguel 1960
The American Journal of CARDIOLOGY
Volume 46
345
in select cases of Prinxmetal’s angina suggests that spasm may be responsible for angina, myocardial infarction, and even sudden death in some patients with hypertrophic obstructive cardiomyopathy.4 The evolution of the role of spasm in hypertrophic obstructive cardiomyopathy is in parallel with its recent development as a pathogenetic mechanism causing chest pain, acute myocardial infarction and possibly sudden death in select patients with the mitral valve prolapse syndrome. Chesler et al5 reported on four patients with the billowing mitral leaflet syndrome and acute myocardial infarction who were subsequently found to have angiographically normal coronary arteries. These authors postulated coronary arterial spasm as the cause. This concept received further support from Buda et al.,6 who found 9 of 10 patients with coronary spasm to have angiographic mitral valve prolapse, although in 8 the spasm occurred at the catheter tip. However, we7 recently encountered four patients with the prolapse-click syndrome who have evidence of spontaneous or ergonovineinduced coronary spasm. Recently, it has been well documented that attacks of variant angina can result in acute myocardial infarction, even in the absence of atherosclerosis. Furthermore, pain appears to be an insensitive measure of the occurrence of coronary spasm as demonstrated by ambulatory monitoring of three patients with variant angina.9 Of 1,045 spontaneous episodes of S-T segment elevation 89 percent were totally asymptomatic. Coronary arterial vasospasm appears to be a significant clinical entity. Its best method of identification and exact contribution to various forms of cardiac disease still remains to be defined. Richard K. Mautner, MD, FACC John H. Phillips, MD, FACC Department of Cardiology Tulane University New Orleans, Louisiana References 1. Muon BJ, f!pmtohs2 Robwfa WC. Hypetlrophk cardiomyopathyand tranamlNal myoolvdtalItWctkn withoutrl@fkant athemscleronisof tha inbnnwai wlonary arterl6s. Am J Can%l1979:49:1089-1102. 2. MWb!8f WC,Than88 f, Dhurdu R, Pftfif@ Jff. F&)ertrophk dx4ructkn cardle myopathyawl ceronuy * spasm.chest, in peas. 3. @odwfn Jf. ?it+SS?fiOCM?ASH. A plea for unity.Am iia.w 1975;39:269-77. 4. fWCfDR,QldcAE.CWmoPR,Quhanuff,HanimnLlCAlkreda&wt#cactfvHy in comnwy mtay spawn. Am J Ctwdlol1979;43:1073-9. 5. ~EuYarE,~JA~af.A~~~~withnomtaicaonary art01W: a poMibk ~ifestatkn of the billowingleafiat syndrome. Clrcuiatkn 1976; 54203-g. 6. SudaYLawnaDGMyum110,~at.Cwmmywteyspe3mandmthivafueprolapse. Am lhft J 1978;95:457-62. 8. W JE. The syn&cmaof vsrbnt angfnaadmhatf~ in acue myotxdtal InfarctIon. chudatkn 1979;59:297-306. 9. RQhon4PIbnonRY.WLrAa~JA.F~OC.V~~~na: IWwkn of Wax08 of sympametk nervoussystemhnct~on.Am J Cardki 1979; 4331090-5.
RIGHT VENTRICULAR
FIGURE 1.
Right ventricular intracavitary recording.
electrocardiogram showed a definite pattern of injury (S-T segment elevations representing a current of injury with the electrode in endocardial contact; Fig. 1). In all three patients a pattern of right ventricular involvement was evident on technetium99m stannous pyrophosphate scanning. Only two of these patients presented with the hemodynamic signs that would usually arouse the suspicion of right ventricular involvement. Moreover, surface electrode recordings over the right precordium revealed no abnormality. An intracavitary electrocardiogram was also recorded in five patients with the sick sinus syndrome who had a temporary pacemaker inserted. The results were a normal intracavitary pattern with an isoelectric S-T segment. Of particular interest is a case of a patient with an extensive anterior myocardial infarction and a right bundle branch block. Intracavitary recordings, made at various sites during pacemaker electrode insertion under fluoroscopic control, showed septal and right ventricular involvement. Technetium-99m stannous pyrophosphate scans suggested only anterior myocardial infarction without hinting at the true extent of the damage. Facilities for nuclear scanning are not always at hand, whereas pacemakers are readily available. It may be useful to perform right ventricular recordings as a routine procedure in all cases in which a pacemaker is indicated. This procedure may unmask right ventricular extension of infarction even in cases in which it may not be hemodynamically obvious nor indicated on technetium-99m pyrophosphate scans. A. Marmor, MD G. Alpan A. Palant, MD Department of Cardiology Carmel Hospital Haifa, Israel
INFARCTION
There has been renewed interest in right ventricular infarction.‘p2 It is clear that a major difficulty lies in the antemortem diagnosis. We wish to report a simple and readily available method that may aid such diagnosis. In six patients with inferior wall myocardial infarction, the appearance of A-V block required the insertion of a temporary pacemaker. Before the electrode was connected to the pulse generator, an intracavitary recording was made by connecting the distal pole of the pacemaker electrode to the chest lead electrode of the electrocardiographic recorder. In three patients the intracavitary
TO THE EDITOR
References 1. bmrJM,Rofmi#WC.Ri@evecrlrlcular intarctknwmpiicatmgleftvelwicularinfarctkn Secondaryto cwonary heart disease. Am J Cardioi1978;42:985-94. 2. f_cetl I), Lof&adl RC. pohal GM, * al. Ri9htventrkxdarInfwctioo.Clinicaldia9noak and differentlatlonfrom cardiactamponadeand pwkardlal oons!xictlon. Am J Cardiol 1979;43:465-71.
Auguel 1960
The American Journal of CARDIOLOGY
Volume 46
345