CLINICAL STUDIES
Exercise-induced abnormal blood pressure responses are related to subendocardial ischemia in hypertrophic cardiomyopathy
Noriko Yoshida, MD*,
Hisao Ikeda, MD*,
Toyofumi Wada, MD*,
Akira Matsumoto, MD*,
Sanae Maki, MD*,
Aiko Muro, MD*,
Akira Shibata, PhD and
Tsutomu Imaizumi, MD, FACC*
* Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan
Department of Public Health, Kurume University School of Medicine, Kurume, Japan
Manuscript received June 9, 1998;
revised manuscript received August 4, 1998,
accepted August 26, 1998.
Address for correspondence: Dr. Hisao Ikeda, Department of Internal Medicine III, Kurume University School of Medicine, 67, Asahi-machi, Kurume, 830-0011 Japan
ikeikeda{at}med.kurume-u.ac.jp
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Abstract
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Objectives. We examined by thallium-201 scintigraphy whether exercise-induced abnormal blood pressure response (BPR) is related to myocardial ischemia.
Background. Hemodynamic instabilities during exercise in patients with hypertrophic cardiomyopathy (HCM) are considered to be caused by abnormal reflex control of vascular resistance.
Methods. In 105 patients with HCM, exercise thallium scintigraphy was performed by means of a multistage, symptom-limited bicycle ergometer exercise test.
Results. Eighty-eight patients had normal BPR ( 25 mm Hg from baseline to peak exercise), and 17 had abnormal BPR (<25 mm Hg). Clinical characteristics including age, the prevalence of obstruction, New York Heart Association functional class and echocardiographic measurements were similar between the two groups. Left ventricular end-diastolic pressure was significantly higher in patients with abnormal BPR than in those with normal BPR (18 ± 8 vs. 14 ± 5 mm Hg, p < 0.05). Exercise-induced perfusion abnormalities including fixed and reversible perfusion defects, and left ventricular cavity dilatation (LVCD) were identified in 72 (69%) of 105 study patients. Left ventricular cavity dilatation indicates subendocardial hypoperfusion and is a marker of diffuse subendocardial ischemia. The prevalence of fixed or reversible perfusion defects was similar between the two groups. Patients with abnormal BPR had the higher prevalence of LVCD as compared to those with normal BPR (47.1 vs. 10%, p < 0.0002). Multiple logistic regression analysis revealed that LVCD was independently associated with abnormal BPR (odds ratio 3.76, 95% confidence interval 1.61 to 8.76).
Conclusions. Exercise-induced abnormal BPRs in patients with HCM are related to subendocardial ischemia during exercise.
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Abbreviations and Acronyms
| | BPR | = blood pressure response | | HCM | = hypertrophic cardiomyopathy | | LVCD | = left ventricular cavity dilatation | | LVEDP | = left ventricular end-diastolic pressure |
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Patients with hypertrophic cardiomyopathy (HCM) have hemodynamic instabilities with abnormal blood pressure response (BPR) during exercise (1,2). The possible mechanism is considered to be due to a fall in systemic vascular resistance during exercise (1,2). Myocardial ischemia commonly occurs in patients with HCM despite normal epicardial coronary arteries. It is possible that abnormal BPRs are related to myocardial ischemia. This issue has never been investigated. Thallium-201 single photon emission computed tomography is a noninvasive method with which we are able to evaluate myocardial ischemia during exercise. Left ventricular cavity dilatation (LVCD) during exercise on thallium scintigrams indicates subendocardial hypoperfusion and is a marker of diffuse subendocardial ischemia (3,4). To assess the relationship between abnormal BPR and subendocardial ischemia in HCM, we therefore performed exercise thallium-201 single photon emission computed tomography in patients with HCM who had normal or abnormal BPRs during exercise testing.
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Methods
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Study patients.
The study population consisted of 105 patients with HCM who were initially diagnosed at the Kurume University Hospital. They were 84 men and 31 women (13 to 77 years old, mean 48 years). The diagnosis of HCM was based on the typical clinical, electrocardiographic and hemodynamic features with echocardiographic demonstration of a nondilated, asymmetrically hypertrophied left ventricle in the absence of other cardiac or systemic diseases that could produce left ventricular hypertrophy (5). In all patients, cardiac catheterization, including left ventricular and selective coronary angiograms and exercise thallium-201 studies, was performed. The following patients were excluded from this study: patients who had valvular heart disease, coronary artery disease with significant atherosclerotic lesion, history of systemic hypertension >160/90 mm Hg and severe symptoms (New York Heart Association functional class IV). These studies were approved by our institutional ethic committees, and informed consent for the study was obtained from all patients.
Exercise thallium single photon emission computed tomographic imaging.
Cardioactive medicines were discontinued at least for five half-lives before the present study. After an overnight fast, exercise thallium scintigraphy was performed by means of a multistage, symptom-limited bicycle ergometer exercise test with continuous monitoring of symptoms, electrocardiogram and heart rate. Systolic blood pressure was periodically measured at 1-min interval at rest, during exercise and during the initial 5 min of the recovery period. Measurements were made by digital palpation of the brachial artery using a mercury sphygmomanometer. At peak exercise, patients intravenously received 3 mCi of thallium-201, and exercise was continued for an additional period of 60 s to allow adequate circulation of the isotope. The exercise test was terminated when there was ischemic ST segment depression >0.2 mV, significant arrhythmia, moderate or severe chest pain, significant hypotension, excessive fatigue, shortness of breath or achievement of 100% of the maximal predicted heart rate. As previously described (6), abnormal BPR was defined as the failure for systolic BPR to increase by 25 mm Hg from the resting value.
Thallium imaging was begun within 10 min of the completion of exercise and repeated after 4 h. The studies were performed with a rotating gamma camera of a wide field of view equipped with a low energy, medium resolution, high sensitivity and parallel hole collimator (RC-1500I, Hitachi) centered on the 70-KeV photopeak with a 10% window. The camera was rotated over a 180° arc in an elliptical orbit about the patient’s anterior thorax from 45° right anterior oblique to 45° left posterior oblique position. Thirty-two images were obtained in a 64 x 64 matrix for 30 s. For image reconstruction, thallium images were processed on an image-analyzing system (RW 3000, Hitachi). Then, reconstruction was performed using a Butterworth filter with a cutoff frequency of 0.25 cycles/pixel and an order of 8. No attenuation or scatter correction was employed.
Image analysis.
The initial and delayed tomographic images were interpreted by three experienced observers who had no knowledge of the present study design. For each study, the observers evaluated two short axis slices (basal and midventricular) and one midvertical long axis slice. The basal and midventricular short axis slices were divided into six segments each. In the vertical long axis slice, one apical segment was chosen. Then, a total of 13 segments per patient were evaluated in this study. The degree of radiotracer uptake for each of the 13 segments was semiquantitatively assessed using a five-point scoring system modified from the previous method (4,7). Regional thallium uptake was graded from 0 to 4, in increments of 1 with a score of 4 signifying normal activity and a score of 0 signifying absent activity. Perfusion abnormalities were defined as fixed or reversible perfusion defects and exercise-induced LVCD. Scores for each segment were averaged; no change from the exercise to the redistribution study was considered a fixed perfusion defect, and a change of 1 or more from the exercise to the redistribution study was considered a reversible perfusion defect. LVCD was assessed qualitatively (4) and determined to be absent or present by independent observers unaware of the study protocol.
Statistical analysis.
Data were expressed as mean value ± SD or percentages. Comparisons between groups of patients were performed with the two-tailed, unpaired Student t test. Differences in proportions were analyzed with the chi-square test or Fisher’s exact test. A multiple logistic regression analysis was performed to assess independent influencing factors for BPR during exercise, with the normal or abnormal BPR as a dependent variable. The following variables were used as possible influencing factors: age, gender, left ventricular outflow obstruction, family history of sudden cardiac death, history of chest pain, cardiothoracic ratio, electrocardiographic and echocardiographic findings, hemodynamic data, and scintigraphic findings. Differences were considered statistically significant when the probability was less than 0.05.
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Results
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Clinical characteristics of patients with normal or abnormal BPR during exercise testing.
Clinical characteristics of patients with normal or abnormal BPRs during exercise testing are shown in Table 1. The two groups did not differ in terms of the age, gender, presence of the left ventricular outflow obstruction, family history, history of chest pain, New York Heart Association functional class, cardiothoracic ratio, electrocardiographic and echocardiographic findings. However, patients with abnormal BPR had greater left ventricular end-diastolic pressure (LVEDP) at rest than those with normal BPR (p < 0.05). Exercise tolerance, heart rate-pressure product and difference between peak and rest systolic blood pressure were significantly lower in patients with abnormal BPR than in patients with normal BPR (p < 0.05).
Thallium-201 emission computed tomography.
Perfusion abnormalities were identified in 72 (69%) of the 105 study patients. Of the perfusion abnormalities, fixed and reversible perfusion defects, and LVCD were observed in 31 (30%), 63 (60%) and 17 patients (16%), respectively. When patients were divided into the two groups of normal or abnormal BPR during exercise testing (Table 2), patients with abnormal BPR had the higher prevalence of LVCD as compared to those with normal BPR (p < 0.0002). However, the two groups did not differ in terms of the fixed or reversible perfusion defects. There were no differences in locations of fixed or reversible perfusion defect between the two groups (data not shown). Of the patients who had both abnormal BPR and perfusion abnormalities, patients (n = 8) with LVCD had more elevated LVEDP as compared to those (n = 5) without LVCD (20 ± 8 vs. 10 ± 2 mm Hg, p < 0.03). Figure 1 shows representative thallium tomographic images of LVCD in a patient with HCM who had abnormal BPR during exercise testing.
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Figure 1 Stress (top) and delayed (bottom) thallium tomographic images of the heart of a patient with hypertrophic cardiomyopathy who had abnormal blood pressure response during exercise testing. Note that stress images demonstrate apparent left ventricular cavity dilatation in the basal, midventricular short axis and vertical long axis slices.
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Multiple logistic regression analysis.
By multiple logistic regression analysis corrected for possible influencing factors, LVCD on thallium scintigraphy was independently associated with abnormal BPR (odds ratio 3.76, 95% confidence interval 1.61 to 8.76, p = 0.0022).
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Discussion
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The major findings of this study were that HCM patients with abnormal BPR during exercise had the greater LVEDP and higher prevalence of LVCD on thallium scintigraphy.
Relation of thallium perfusion abnormalities to abnormal BPR during exercise.
We assessed myocardial perfusion abnormalities during exercise with thallium scintigraphy in patients with HCM. Previous studies have shown that the prevalence of perfusion abnormalities ranges from 52 to 74% in patients with HCM (4,8,9). In the present study, the prevalence of perfusion abnormalities, including perfusion defects (fixed and reversible) and LVCD, was 69%. Thus, the present study confirms that perfusion abnormalities are common in patients with HCM. It is generally considered in patients with HCM that fixed perfusion defects may represent regional myocardial fibrosis and scarring (8,10), whereas reversible perfusion defects may represent regional myocardial ischemia (4,8,9). Although many patients had fixed or reversible perfusion defects in the present study, these perfusion abnormalities were not due to coronary artery disease of large epicardial arteries, because all patients had normal epicardial coronary arteries by coronary angiography. Therefore, the genesis of these regional perfusion abnormalities was not clarified in this study. In the present study, the prevalence of either fixed or reversible perfusion defect was similar between the patient groups with normal and abnormal BPRs. Thus, it is unlikely that abnormal BPR in HCM was related to regional myocardial fibrosis, scarring or ischemia.
LVCD assessed by thallium scintigraphy indicates ischemia-related subendocardial hypoperfusion, because this scintigraphic abnormality occurs in the absence of any significant changes in left ventricular cavity size by radionuclide angiography (4). Previous studies have shown that LVCD on thallium scintigraphy is an indication of severe multivessel disease in patients with coronary artery disease (3). Scintigraphic findings of LVCD are supported by the concordance of lactate metabolic abnormalities during pacing stress in HCM (4). Thus, although we have no other evidence of myocardial ischemia, it is likely that LVCD indicates diffuse subendocardial ischemia in our study patients. The mechanisms responsible for subendocardial ischemia in HCM are unknown. Proposed possible mechanisms are structural abnormalities of intramural small coronary arteries (11,12), distribution of fibrous and hypertrophied tissue formation in the left ventricular myocardium (13), limitation of coronary flow reserve (14–16), impairment of diastolic filling (17,18) and presence of left ventricular outflow obstruction (19,20). These histologic and hemodynamic abnormalities could potentially induce inadequacy of myocardial blood flow and increase in myocardial oxygen demand during exercise stress, resulting in subendocardial ischemia. Although we did not specifically examined mechanisms of subendocardial ischemia in this study, left ventricular obstruction was not likely, because the prevalence of obstruction was similar between patients with LVCD and without LVCD (10% vs. 12%). It is possible that impairment of diastolic filling was responsible, because LVEDP was higher in patients with LVCD than in those without LVCD (20 ± 8 vs. 10 ± 2 mm Hg). However, this was speculative, because we did not measure LVEDP during exercise in this study.
Possible role of subendocardial ischemia in exercise-induced abnormal BPR.
It has been proposed that the mechanism of exercise-induced abnormal BPR is due to abnormalities of vascular function in systemic vascular resistance during exercise stress (1,2). In this study, abnormal BPR was unlikely due to systolic dysfunction or left ventricular obstruction, because fractional shortening and the prevalence of obstruction were similar between the patients with and without abnormal BPRs. The relation of exercise-induced abnormal BPR to myocardial ischemia in HCM has not been investigated. In the present study, patients with abnormal BPR had the significantly higher prevalence of LVCD as compared to those with normal BPR. The two groups did not differ in terms of the fixed or reversible perfusion defect. Thus, these findings indicate that exercise-induced abnormal BPR are related to diffuse subendocardial ischemia rather than regional myocardial fibrosis and scarring or ischemia. The patients with abnormal BPR had the higher LVEDP at rest. Cannon et al have demonstrated significant elevations in LVEDP after pacing stress in patients with LVCD during exercise test (4). Thus, it is feasible to think that patients with abnormal BPR had even higher filling pressures during exercise, resulting in less coronary perfusion pressure, which would cause diffuse subendocardial ischemia. Therefore, the present findings suggest that, in patients with LVCD, exercise-induced abnormal BPR may be related to development of subendocardial ischemia in association with further elevation in LVEDP during exercise.
It is not clear from our study how subendocardial ischemia and abnormal BPR are related. It has been reported that cardiac output is normal during exercise in HCM patients with abnormal BPR (1). Thus, it is not likely that ischemia-induced cardiac dysfunction with low cardiac output contributed to abnormal BPR. A previous study by Lele et al has demonstrated that an abnormal vasodilator response, which is caused by a centrally mediated reflex triggered by ventricular baroreceptor stimulation, may be the cause of exercise-induced hypotension in some patients with ischemic heart disease (21). These findings suggest that myocardial ischemia may be one of the stimuli responsible for the reflex-mediated vasodilator response. Accordingly, ischemia-induced abnormal neurocardiogenic reflex may have played a role in abnormal BPR in our patients. This possibility needs to be further investigated. On the contrary, it is possible that exercise-induced abnormal BPR (hypotension) may have aggravated ongoing myocardial ischemia during exercise.
Limitations.
In the present study, systolic blood pressure during exercise testing was measured by digital palpation of the brachial artery. Accordingly, palpation of blood pressure might have led to erroneous measurements, particularly during strenuous exercise.
Clinical implications.
The present study provides several clinical implications. Evidence of inducible ischemia by thallium scintigraphy has been shown to be related to a history of cardiac arrest or syncope (22), and to potentially lethal arrhythmias (23), which are risk factors for sudden cardiac death in patients with HCM. Recently, we and others have demonstrated that exercise-induced abnormal BPR is a strong predictor for sudden cardiac death in HCM (6,24). Furthermore, the present study has shown that LVCD is independently associated with abnormal BPR. Taken together, scintigraphic evidence of LVCD associated with exercise-induced abnormal BPR in HCM patients may be useful for identifying high risk patients for sudden cardiac death.
Conclusions.
The present study demonstrated for the first time that exercise-induced abnormal BPR may be related to the development of subendocardial ischemia in patients with HCM. Our findings may contribute to understanding of the pathophysiologic association between myocardial ischemia and altered exercise hemodynamics in HCM.
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Footnotes
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This study was supported by a research grant for intractable disease from the Ministry of Health and Welfare of Japan, Tokyo, Japan.
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References
|
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1. Frenneaux MP, Counihan PJ, Caforio ALP, Chikamori T, McKenna WJ. Abnormal blood pressure response during exercise in hypertrophic cardiomyopathy. Circulation. 1990;82:1995–2002[Abstract/Free Full Text]
2. Counihan PJ, Frenneaux MP, Webb DJ, McKenna WJ. Abnormal vascular responses to supine exercise in hypertrophic cardiomyopathy. Circulation. 1991;84:686–696[Abstract/Free Full Text]
3. Ritchie J, Bateman T, Bonow R, et al. Guidelines for clinical use of cardiac radionuclide imaging: a report of the American Heart Association/American College of Cardiology task force on assessment of diagnostic and therapeutic cardiovascular procedures, committee on radionuclide imaging, developed in collaboration with the American Society of Nuclear Cardiology. Circulation. 1995;91:1278–1303
4. Cannon RO, Dilsizian V, O’gara PT, et al. Myocardial metabolic, hemodynamic, and electrocardiographic significance of reversible thallium-201 abnormalities in hypertrophic cardiomyopathy. Circulation. 1991;83:1660–1667[Abstract/Free Full Text]
5. Maron BJ, Epstein SE. Hypertrophic cardiomyopathy: a discussion of nomenclature. Am J Cardiol. 1979;43:1242–1244[CrossRef][Medline]
6. Maki S, Ikeda H, Muro A, et al. Predictors of sudden cardiac death in hypertrophic cardiomyopathy. Am J Cardiol. 1998;82:774–778[CrossRef][Medline]
7. Okada RD, Boucher CA, Kirshenbaum HK, et al. Improved diagnostic accuracy of thallium-201 stress test using multiple observers and criteria derived from interobserver analysis of variance. Am J Cardiol. 1980;46:619–624[Medline]
8. O’gara PT, Bonow RO, Maron BJ, et al. Myocardial perfusion abnormalities in patients with hypertrophic cardiomyopathy: assessment with thallium-201 emission computed tomography. Circulation. 1987;76:1214–1223[Abstract/Free Full Text]
9. Udelson JE, Bonow RO, O’Gara PT, et al. Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy. Circulation. 1989;79:1052–1060[Abstract/Free Full Text]
10. Nagata S, Park Y, Minamikawa T, et al. Thallium perfusion and cardiac enzyme abnormalities in patients with familial hypertrophic cardiomyopathy. Am Heart J. 1985;109:1317–1322[CrossRef][Medline]
11. Maron B, Epstein S, Roberts W. Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. Am J Cardiol. 1979;43:1086–1102[CrossRef][Medline]
12. Maron BJ, Wolfson JK, Epstein SE, Roberts WC. Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy. J Am Coll Cardiol. 1986;8:545–557[Abstract]
13. Opherk D, Mall G, Zebe H, et al. Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries. Circulation. 1984;69:71–79
14. Cannon RO, Rosing DR, Maron BJ, et al. Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures. Circulation. 1985;71:234–243[Abstract/Free Full Text]
15. Ogata Y, Hiyamuta K, Terasawa M, et al. Relationship of exercise or pacing induced ST segment depression and myocardial lactate metabolism in patients with hypertrophic cardiomyopathy. Jpn Heart J. 1986;27:145–158[Medline]
16. Ikeda H, Shimamatsu M, Yoshiga O, Shibao K, Koga Y, Toshima H. Impaired myocardial perfusion in patients with hypertrophic cardiomyopathy: assessment with digital subtraction coronary arteriography. Heart Vessels. 1988;4:170–178[Medline]
17. Brutsaert D, Rademakers F, Sys S. Triple control of relaxation: implications in cardiac disease. Circulation. 1984;69:190–196[Free Full Text]
18. Bonow RO, Dilsizian V, Rosing DR, Maron BJ, Bacharach SL, Green MV. Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects. Circulation. 1985;72:853–864[Abstract/Free Full Text]
19. Wigle E, Sasson Z, Henderson M, et al. Hypertrophic cardiomyopathy: the importance of the site and the extent of hypertrophy. A review. Prog Cardiovasc Dis. 1985;28:1–83[CrossRef][Medline]
20. Cannon RO, Schenke WH, Maron BJ, et al. Differences in coronary flow and myocardial metabolism at rest and during pacing between patients with obstructive and patients with nonobstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 1987;10:53–62[Abstract]
21. Lele SS, Scalia G, Thomson H, et al. Mechanism of exercise hypotension in patients with ischemic heart disease. Role of neurocardiogenically mediated vasodilation. Circulation. 1994;90:2701–2709[Abstract/Free Full Text]
22. Dilsizian V, Bonow RO, Epstein SE, Fananapazir L. Myocardial ischemia detected by thallium scintigraphy is frequently related to cardiac arrest and syncope in young patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 1993;22:796–804[Abstract]
23. von Dohlen TW, Prisant LM, Frank MJ. Significance of positive or negative thallium-201 scintigraphy in hypertrophic cardiomyopathy. Am J Cardiol. 1989;64:498–503[CrossRef][Medline]
24. Sadoul N, Prasad K, Elliot PM, Bannerjee S, Frenneaux MP, McKenna WJ. Prospective prognostic assessment of blood pressure response during exercise in patients with hypertrophic cardiomyopathy. Circulation. 1997;96:2987–2991[Abstract/Free Full Text]
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Abstract
Methods