READERS’ COMMENTS
Effects of Nifedipine on Total lschemic Activity in Angina and the Importance of InHospital Psychological Stress in Myocardial Infarction
in ischemic eventsin stable angina’; however, alleviation of spasmof resistance vessel does not contradict any concomitant nifedipine-induced reduction of myocardial oxygen demand by lowering systolic blood pressure.’ If, indeed, spasm of resistance vesselis involved with morning ischemic episodes, this might be important evidencefor the theory; myocardial infarctions and sudden cardiac death have a circadian rhythm generally similar to angina, and the concept assumes that coronary artery diseaseis one disorder due to spasmof resistance vessel.4 The second study2 reported that patients with acute myocardial infarction who had in-hospital symptoms of psychological stresshad an almost threefold increased risk of cardiac death over 5 years, and such evidence of an important role for stress in coronary artery diseaseis in keeping with an important role for spasmof resistancevesselin this disorder. The ability of stress to trigger silent episodesof ischemia2 is evidence for a direct connection between stress and ischemia, and stress-induced spasm of resistance vessel seems possible as centrally mediated vasoconstriction of resistance vesselscan occur.(j The findings of the 2 studies are only consistent with the spasm of resistancevesselconcept and might be explained by other models for coronary artery disease. Alternate paradigms are tested by determining whether they explain eventsbetter than other positions and without inconsistencies, and the view that coronary artery diseaseis one disorder caused by spasm of resistance vessel appears to well explain the findings of the 2 studies.
The findings of 2 recent reports1,2 do not seemwell explained by standard views about coronary artery disease, but appear to be highly consistent with the spasm of resistance vessel concept, which is regarded as an alternate paradigm or model to explain this disorder. The concept, first described in 19733 and recently updated,4 asserts that symptoms in coronary artery disease are due to primary spasm of resistance vessel. This spasm is regarded as “inappropriate” activation of preexisting autoregulatory mechanisms by disease states, which can be regarded as risk factors. Many risk factors can readily be related to spasm of resistance vessel, such as emotional stress, cold and cocaine usage, and severe coronary artery diseaseis presumed to cause spasm of resistance vessel through the sequenceof severeischemia, ischemic tissue injury and injury-induced spasm of resistance vessel. Occlusions in epicardial arteries are given other roles: Coronary artery disease causes ischemia-induced spasm of resistance vessel, spasm in epicardial arteries is reflex to spasmof resistance vessel, and thromboses are secondary to the stasis of spasm of resistance vesseland to reflex spasmin epicardial arteries, which can cause plaque rupture. The first report’ described nifedipine-induced suppression of morning ischemic activity and improvement of exercisetreadmill testing in casesof angina, and both findings H. Richard Hellstrom, MD are consistent with the alleviation Syracuse,New York of spasm of resistance vessel by va25 February 1991 sodilation. Resistance vessels are more constricted at 9:00 A.M.,~ and 1. Nesto RW, Phillips RT, Kett KG, there is evidence that constriction McAuliffe LS, Roberts M, Hegarty P. of the microcirculation is involved Effect of nifedipine on total ischemic acLetters (from the United States) concerning a particular article in the J~urnai must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
tivity and circadian distribution of myocardial ischemic episodes in angina pectoris. Am J Cardiol 1991;67:128-132. 2. Frasure-Smith N. In-hospital symptoms of psychological stress as predictors of long-term outcome after acute myocardial infarction in men. Am J CardioE
1991;67:121-127. 3. Hellstrom HR. Vasospasm in ischemic heart disease: a hypothesis. Perspect Biol Med 1973;16:427-440. 4. Hellstrom HR. The spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases. Med Hypotheses 1990;33:31-41. 5. Fujita M, Franklin D. Diurnal changes in coronary blood flow in conscious dogs. Circulation 1987;76:488-491. 6. Shepherd JT, Dembroski TM, Brody MJ, Dimsdale JE, Eliot RS, Light KC, Miller NE, Myers HF, Obrist PA, Schneiderman N, Skinner JE, Williams RB Jr. Task Force 3: biobehavioral mechanisms in coronary artery disease: acute stress. Circulation 1987;76(suppl I):I150-I-157.
Systolic Excursion of the Mitral Anulus as an Index of Left Ventricular Systolic Function We would like to comment on the report by Pai et al’ in the January issue of the Journal on the usefulnessof the systolic excursion of the mitral anulus as an index of left ventricular (LV) systolic function. These investigators demonstrated that the systolic excursion of the mitral anulus measured from the apical 4-chamber view is strongly related to the LV systolic ejection measured by radionuclide technique. They indicate as the major drawback that the movement of the apex is not taken into account, as only the movement of the mitral anulus in relation to the transducer is considered.We feel that this is not a drawback, because we have found that the apex remains in a stable position during systole while the LV base moves towards the apex.2 The basal excursion should be adjusted for heart size. This can be done by normalizing for the LV long-axis measured in the same view at end diastole. The authors found that the systolic excursion of the mitral anulus was a better correlate of radionuelide LV ejection fraction than LV fractional shortening or ejection fraction by echocardiography using the method described by Teichholz et a1.3They suggestedthat this may be partly due to the fact that a sizeREADERS’ COMMENTS
829
able proportion of the patients had regional wall motion abnormalities of the left ventricle. We agree with these conclusions. We expect, however, that a new echocardiographic method would provide a better correlation with radionuclide LV ejection fraction. The influence of regional wall motion abnormalities on LV ejection fraction is taken into consideration when the measurement of the excursion of the mitral anulus is complemented with tracing of the endocardial borders at end diastole and end systole at endexpiration. This addition would cost little extra effort. The combined measurement of systolic excursion of the mitral anulus and displacement of the endocardial borders can be assessedwith a small measurement variability using a new algorithm, recently described and validated by our group.4 Patricia E. Assmann, MD Cornelis J. Slager, MSE Jos R. Roelandt, MD
Rotterdam, The Netherlands 12 March 1991 1. Pai RG, BodenheimerMM, Pai SM, KossJH, Adamick RD. Usefulnessof systolic excursion of the mitral anulus as an index of left ventricular systolic function. Am J Cardiol 1991;67:222-224. 2. AssmannPE, Slager CJ, DreysseST, van der BordenSG, OomenJA, Roelandt JR. Two-dimensional echocardiographic analysis of the dynamic geometry of the left ventricle: the basis for an improved model of wall motion. J Am Sot Echo 1988;1:393-405. 3. Teichholz LE, Keulen T, Herman MV, Gorlin R. Problemsin echocardiographic volume determinations:echocardiographic-angiographic correlations in the presenceor absenceof asynergy.Am J Cardiol 1976;37:7-11. 4. AssmannPE, Slager CJ, van der BordenSG, DreysseST, TijssenJGP,Sutherland GR, RoelandtJR. Quantitative analysis of global and regional left ventricular function-a problem revisited. J Am Sot Echo 1990;3:478-487.
Anticardiolipin Antibody liters in Patients with Myocardial Infarction
Caterina et al1 reported that anticardiolipin antibody (ACA) was present at low titer in 43% of patients with coronary artery disease (CAD) although low titers were 830
also present in a similar number of normal subjects. Kiemp et al2 had previously reported that ACA titers were raised in 80.2% of CAD patients on L 1 occasion during a 1 to 11 day hospital admission and that the CAD patients had significantly higher titers than were seen in groups of patients with tuberculosis and rheumatoid arthritis. Hamsten et al3had earlier reported that elevated ACA levels were associatedwith the subsequent development of cardiovascular events in a cohort of patients
Effects of Nifedipine on Total lschemic Activity in Angina and the Importance of InHospital Psychological Stress in Myocardial Infarction
in ischemic eventsin stable angina’; however, alleviation of spasmof resistance vessel does not contradict any concomitant nifedipine-induced reduction of myocardial oxygen demand by lowering systolic blood pressure.’ If, indeed, spasm of resistance vesselis involved with morning ischemic episodes, this might be important evidencefor the theory; myocardial infarctions and sudden cardiac death have a circadian rhythm generally similar to angina, and the concept assumes that coronary artery diseaseis one disorder due to spasmof resistance vessel.4 The second study2 reported that patients with acute myocardial infarction who had in-hospital symptoms of psychological stresshad an almost threefold increased risk of cardiac death over 5 years, and such evidence of an important role for stress in coronary artery diseaseis in keeping with an important role for spasmof resistancevesselin this disorder. The ability of stress to trigger silent episodesof ischemia2 is evidence for a direct connection between stress and ischemia, and stress-induced spasm of resistance vessel seems possible as centrally mediated vasoconstriction of resistance vesselscan occur.(j The findings of the 2 studies are only consistent with the spasm of resistancevesselconcept and might be explained by other models for coronary artery disease. Alternate paradigms are tested by determining whether they explain eventsbetter than other positions and without inconsistencies, and the view that coronary artery diseaseis one disorder caused by spasm of resistance vessel appears to well explain the findings of the 2 studies.
The findings of 2 recent reports1,2 do not seemwell explained by standard views about coronary artery disease, but appear to be highly consistent with the spasm of resistance vessel concept, which is regarded as an alternate paradigm or model to explain this disorder. The concept, first described in 19733 and recently updated,4 asserts that symptoms in coronary artery disease are due to primary spasm of resistance vessel. This spasm is regarded as “inappropriate” activation of preexisting autoregulatory mechanisms by disease states, which can be regarded as risk factors. Many risk factors can readily be related to spasm of resistance vessel, such as emotional stress, cold and cocaine usage, and severe coronary artery diseaseis presumed to cause spasm of resistance vessel through the sequenceof severeischemia, ischemic tissue injury and injury-induced spasm of resistance vessel. Occlusions in epicardial arteries are given other roles: Coronary artery disease causes ischemia-induced spasm of resistance vessel, spasm in epicardial arteries is reflex to spasmof resistance vessel, and thromboses are secondary to the stasis of spasm of resistance vesseland to reflex spasmin epicardial arteries, which can cause plaque rupture. The first report’ described nifedipine-induced suppression of morning ischemic activity and improvement of exercisetreadmill testing in casesof angina, and both findings H. Richard Hellstrom, MD are consistent with the alleviation Syracuse,New York of spasm of resistance vessel by va25 February 1991 sodilation. Resistance vessels are more constricted at 9:00 A.M.,~ and 1. Nesto RW, Phillips RT, Kett KG, there is evidence that constriction McAuliffe LS, Roberts M, Hegarty P. of the microcirculation is involved Effect of nifedipine on total ischemic acLetters (from the United States) concerning a particular article in the J~urnai must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
tivity and circadian distribution of myocardial ischemic episodes in angina pectoris. Am J Cardiol 1991;67:128-132. 2. Frasure-Smith N. In-hospital symptoms of psychological stress as predictors of long-term outcome after acute myocardial infarction in men. Am J CardioE
1991;67:121-127. 3. Hellstrom HR. Vasospasm in ischemic heart disease: a hypothesis. Perspect Biol Med 1973;16:427-440. 4. Hellstrom HR. The spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases. Med Hypotheses 1990;33:31-41. 5. Fujita M, Franklin D. Diurnal changes in coronary blood flow in conscious dogs. Circulation 1987;76:488-491. 6. Shepherd JT, Dembroski TM, Brody MJ, Dimsdale JE, Eliot RS, Light KC, Miller NE, Myers HF, Obrist PA, Schneiderman N, Skinner JE, Williams RB Jr. Task Force 3: biobehavioral mechanisms in coronary artery disease: acute stress. Circulation 1987;76(suppl I):I150-I-157.
Systolic Excursion of the Mitral Anulus as an Index of Left Ventricular Systolic Function We would like to comment on the report by Pai et al’ in the January issue of the Journal on the usefulnessof the systolic excursion of the mitral anulus as an index of left ventricular (LV) systolic function. These investigators demonstrated that the systolic excursion of the mitral anulus measured from the apical 4-chamber view is strongly related to the LV systolic ejection measured by radionuclide technique. They indicate as the major drawback that the movement of the apex is not taken into account, as only the movement of the mitral anulus in relation to the transducer is considered.We feel that this is not a drawback, because we have found that the apex remains in a stable position during systole while the LV base moves towards the apex.2 The basal excursion should be adjusted for heart size. This can be done by normalizing for the LV long-axis measured in the same view at end diastole. The authors found that the systolic excursion of the mitral anulus was a better correlate of radionuelide LV ejection fraction than LV fractional shortening or ejection fraction by echocardiography using the method described by Teichholz et a1.3They suggestedthat this may be partly due to the fact that a sizeREADERS’ COMMENTS
829
able proportion of the patients had regional wall motion abnormalities of the left ventricle. We agree with these conclusions. We expect, however, that a new echocardiographic method would provide a better correlation with radionuclide LV ejection fraction. The influence of regional wall motion abnormalities on LV ejection fraction is taken into consideration when the measurement of the excursion of the mitral anulus is complemented with tracing of the endocardial borders at end diastole and end systole at endexpiration. This addition would cost little extra effort. The combined measurement of systolic excursion of the mitral anulus and displacement of the endocardial borders can be assessedwith a small measurement variability using a new algorithm, recently described and validated by our group.4 Patricia E. Assmann, MD Cornelis J. Slager, MSE Jos R. Roelandt, MD
Rotterdam, The Netherlands 12 March 1991 1. Pai RG, BodenheimerMM, Pai SM, KossJH, Adamick RD. Usefulnessof systolic excursion of the mitral anulus as an index of left ventricular systolic function. Am J Cardiol 1991;67:222-224. 2. AssmannPE, Slager CJ, DreysseST, van der BordenSG, OomenJA, Roelandt JR. Two-dimensional echocardiographic analysis of the dynamic geometry of the left ventricle: the basis for an improved model of wall motion. J Am Sot Echo 1988;1:393-405. 3. Teichholz LE, Keulen T, Herman MV, Gorlin R. Problemsin echocardiographic volume determinations:echocardiographic-angiographic correlations in the presenceor absenceof asynergy.Am J Cardiol 1976;37:7-11. 4. AssmannPE, Slager CJ, van der BordenSG, DreysseST, TijssenJGP,Sutherland GR, RoelandtJR. Quantitative analysis of global and regional left ventricular function-a problem revisited. J Am Sot Echo 1990;3:478-487.
Anticardiolipin Antibody liters in Patients with Myocardial Infarction
Caterina et al1 reported that anticardiolipin antibody (ACA) was present at low titer in 43% of patients with coronary artery disease (CAD) although low titers were 830
also present in a similar number of normal subjects. Kiemp et al2 had previously reported that ACA titers were raised in 80.2% of CAD patients on L 1 occasion during a 1 to 11 day hospital admission and that the CAD patients had significantly higher titers than were seen in groups of patients with tuberculosis and rheumatoid arthritis. Hamsten et al3had earlier reported that elevated ACA levels were associatedwith the subsequent development of cardiovascular events in a cohort of patients
