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Peter Collins - One of the best experts on this subject based on the ideXlab platform.
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abnormal subendocardial perfusion in cardiac Syndrome X detected by cardiovascular magnetic resonance imaging
The New England Journal of Medicine, 2002Co-Authors: Jonathan R Panting, Peter D Gatehouse, Guangzhong Yang, Frank Grothues, David N Firmin, Peter Collins, Dudley J PennellAbstract:A BSTRACT Background In cardiac Syndrome X (a Syndrome characterized by typical angina, abnormal eXercisetest results, and normal coronary arteries), conventional investigations have not found that chest pain is due to myocardial ischemia. Magnetic resonance techniques have higher resolution and therefore may be more sensitive. Methods We performed myocardial-perfusion cardiovascular magnetic resonance imaging in 20 patients with Syndrome X and 10 matched controls, both at rest and during an infusion of adenosine. Quantitative perfusion analysis was performed by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion indeX and the myocardial-perfusion reserve indeX (defined as the ratio of the myocardial perfusion indeX during stress to the indeX at rest). Results In the controls, the myocardial perfusion indeX increased in both myocardial layers with adenosine (in the subendocardium, from a mean [±SD] of 0.12±0.03 to 0.16±0.03 [P=0.02]; in the subepicardium, from 0.11±0.02 to 0.17±0.05 [P=0.002]); in patients with Syndrome X, the myocardial perfusion indeX did not change significantly in the subendocardium (0.13±0.02 vs. 0.14±0.03, P=0.11; P=0.09 as compared with controls) but increased in the subepicardium (from 0.11±0.02 to 0.20±0.04, P<0.001; P=0.11 for the comparison with controls). Adenosine provoked chest pain in 95 percent of patients with Syndrome X and 40 percent of controls (P<0.001). Conclusions In patients with Syndrome X, cardiovascular magnetic resonance imaging demonstrates subendocardial hypoperfusion during the intravenous administration of adenosine, which is associated with intense chest pain. These data support the notion that the chest pain may have an ischemic cause. (N Engl J Med 2002;346:1948-53.)
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abnormal subendocardial perfusion in cardiac Syndrome X detected by cardiovascular magnetic resonance imaging
The New England Journal of Medicine, 2002Co-Authors: Jonathan R Panting, Peter D Gatehouse, Guangzhong Yang, Frank Grothues, David N Firmin, Peter Collins, Dudley J PennellAbstract:Background In cardiac Syndrome X (a Syndrome characterized by typical angina, abnormal eXercise-test results, and normal coronary arteries), conventional investigations have not found that chest pain is due to myocardial ischemia. Magnetic resonance techniques have higher resolution and therefore may be more sensitive. Methods We performed myocardial-perfusion cardiovascular magnetic resonance imaging in 20 patients with Syndrome X and 10 matched controls, both at rest and during an infusion of adenosine. Quantitative perfusion analysis was performed by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion indeX and the myocardial-perfusion reserve indeX (defined as the ratio of the myocardial perfusion indeX during stress to the indeX at rest). Results In the controls, the myocardial perfusion indeX increased in both myocardial layers with adenosine (in the subendocardium, from a mean [±SD] of 0.12±0.03 to 0.16±0.03 [P=0.02]; in the subepicardium, from 0.11±0.02...
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esterified estrogens combined with methyltestosterone improve emotional well being in postmenopausal women with chest pain and normal coronary angiograms
Menopause, 2001Co-Authors: Dawn L Adamson, Carolyn M Webb, Peter CollinsAbstract:Objective The cardiac Syndrome X is described as the triad of angina pectoris, a positive eXercise test for myocardial ischemia, and angiographically smooth coronary arteries. Although Syndrome X does not result in an increased risk of cardiovascular mortality, the symptoms are often troublesome and unresponsive to conventional antianginal therapy. The majority of patients are postmenopausal, and estrogen therapy can alleviate anginal symptoms. We investigated the effect of esterified estrogens combined with methyltestosterone (Estratest) on quality of life in postmenopausal women with Syndrome X. Design Patients were withdrawn from antianginal therapy. Sublingual nitrates were allowed for treatment of anginal episodes. Patients underwent treadmill testing, and quality of life was assessed by using the Short Form-36 and Cardiac Health Profile questionnaires after the women had received 8 weeks of Estratest or identical placebo in a randomized, double-blind, cross-over study. Results Nineteen patients were randomized, and 16 patients completed the protocol. Plasma 17β-estradiol concentrations were significantly increased by Estratest; however, total testosterone levels were not. The “emotional” score of the Cardiac Health Profile questionnaire was significantly improved after Estratest use compared with placebo (p = 0.03); however, there was no significant change in the Short Form-36 questionnaire for any variable. Estratest significantly increased systolic blood pressure and rate pressure product at rest but had no effect on eXercise parameters. Time to onset of chest pain during eXercise was also unaffected. Conclusions We have demonstrated a beneficial effect of Estratest on emotional well-being in postmenopausal women with cardiological Syndrome X. There was no significant treatment effect on eXercise parameters, including time to onset of chest pain.
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cardiac Syndrome X clinical characteristics and left ventricular function long term follow up study
Journal of the American College of Cardiology, 1995Co-Authors: Juan Carlos Kaski, Attilio Maseri, Peter Collins, Petros Nihoyannopoulos, Philip A Poolewilson, Giuseppe M C RosanoAbstract:Objectives. Our aim was to study the clinical characteristics and evolution of symptoms and left ventricular function in a clinically homogeneous group of patients with Syndrome X (angina pectoris, positive eXercise test results and normal coronary arteriograms). Background. The Syndrome of angina with normal coronary arteriograms is heterogeneous and encompasses different pathogenetic entities. These characteristics may contribute to the eXisting controversy concerning the cause of Syndrome X. Methods. We studied 99 patients with Syndrome X (78 women, 21 men; mean age ± SD 48.5 ± 8 years). All underwent clinical characterization, ambulatory electrocardiographic (ECG) monitoring and echocardiographic assessment of left ventricular function during a follow-up period of 7 ± 4 years. Results. The Syndrome was more common in women than in men. Of the women, 61.5% were postmenopausal before the onset of chest pain. All 99 patients had eXertional angina, and 41 also had rest angina. The average duration of episodes of chest pain was > 10 min in 53% of patients. Sublingual nitrate was effective for relief of pain in 42% of patients. Transient ST segment depression was observed during ambulatory ECG monitoring in 64 patients and myocardial perfusion abnormalities in 22. During the first stage of the eXercise test, 32 patients had an increase > 20 mm Hg in systolic blood pressure and showed an earlier onset of ST depression and shorter eXercise time than did patients whose blood pressure increased ≤20%. During follow-up, no deaths or myocardial infarctions occurred, ventricular function was unchanged (shortening fraction 35.4 ± 4% vs. 35.6 ± 3%; heart failure developed in only one patient), systemic hypertension occurred in eight patients and conduction disturbances in four. Symptoms lessened in 11 patients, were variable or unchanged in 64 and worsened in 24. Conclusions. Syndrome X, as defined in this study, occurs predominantly in postmenopausal women. Patients usually have chest pain typical for angina, but conventional antianginal treatment is not often successful. Myocardial perfusion abnormalities occur in a small proportion of patients. Long-term survival is not adversely affected, and deterioration of cardiac function rarely occurs.
Juan Carlos Kaski - One of the best experts on this subject based on the ideXlab platform.
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increased coronary vasoconstrictor response to acetylcholine in women with chest pain and normal coronary arteriograms cardiac Syndrome X
Clinical Research in Cardiology, 2012Co-Authors: Peter Ong, Gabor Borgulya, Anastasios Athanasiadis, Heiko Mahrholdt, Udo Sechtem, Juan Carlos KaskiAbstract:Aims Cardiac Syndrome X (CSX) is characterized by eXercise-induced angina, positive eXercise stress-test responses and angiographically normal coronary arteries. The condition characteristically affects more women than men and is often associated with coronary microvascular dysfunction, i.e., abnormal vasodilatory responses. Recent clinical observations suggest that increased coronary vasoconstriction may have a pathogenic role in CSX. We therefore sought to assess the prevalence of increased epicardial and microvascular coronary vasoconstriction in women with CSX.
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obesity inflammation and brachial artery flow mediated dilatation therapeutic targets in patients with microvascular angina cardiac Syndrome X
Cardiovascular Drugs and Therapy, 2012Co-Authors: Peter Ong, Ramyya Sivanathan, Gabor Borgulya, Mukhtar Bizrah, Yassir Iqbal, Joycelyn Andoh, David Gaze, Juan Carlos KaskiAbstract:Background The pathophysiology of microvascular angina (cardiac Syndrome X, CSX), (effort-induced angina, a positive response to eXercise stress testing and angiographically normal coronary arteries) has not been fully elucidated. Various pathogenic mechanisms have been proposed, amongst which coronary microvascular dysfunction features prominently. Management of patients with microvascular angina is often challenging as a substantial number of patients does not respond to conventional anti-anginal therapy. In this study, we sought to assess the association between brachial artery FMD, high-sensitive C-reactive protein (hs-CRP) and cardiovascular risk factors including obesity in patients with cardiac Syndrome X.
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pathophysiology and management of patients with chest pain and normal coronary arteriograms cardiac Syndrome X
Circulation, 2004Co-Authors: Juan Carlos KaskiAbstract:Patients with cardiac Syndrome X (CSX)—typical chest pain and electrocardiographic changes suggestive of myocardial ischemia despite normal coronary arteriograms–represent a diagnostic and therapeutic riddle. CSX is not associated with an increased mortality or an increased risk of cardiovascular events, but it often severely impairs quality of life and represents a substantial cost burden to the healthcare system. This Syndrome of chest pain with normal coronary arteries encompasses a variety of pathogenic subgroups and is predominantly seen in postmenopausal women. Lack of understanding of the Syndrome by the cardiovascular physician not infrequently results in discounting the clinical problem. Treatment remains elusive, but management strategies can improve the patient’s quality of life and reduce the financial burden imposed on health services. ### Case Report: A 55-year-old white female pharmacist underwent diagnostic coronary arteriography for the assessment of typical eXertional chest pain, which had started 18 months previously and had gradually become more frequent and severe despite treatment with oral and sublingual nitrates and atenolol (50 mg daily). Central chest pain and dyspnea occurred at rest and with emotional stress and responded rather poorly to sublingual nitrate administration. ECG eXercise stress test was positive (Figure 1), and transient perfusion defects were found on thallium-201 dipyridamole testing (Figure 2). She had long-lasting eXcruciating chest pain after dipyridamole infusion. Risk factors included a family history of coronary artery disease, a low-density lipoprotein-cholesterol level of 4.2 mmol/L, a high-density lipoprotein-cholesterol level 0.9 mmol/L, menopausal status, a previous history of smoking, body-mass indeX of 28 kg/m2, and raised high-sensitivity C-reactive protein levels (3.8 mg/L). Coronary arteries and left ventricular function were completely normal. Coronary intravascular ultrasound showed no significant subangiographic disease. After reassurance by her cardiologist, all cardiac medications were discontinued. Symptoms continued to deteriorate over the ensuing months, however, to the point that she was unable to …
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cardiac Syndrome X clinical characteristics and left ventricular function long term follow up study
Journal of the American College of Cardiology, 1995Co-Authors: Juan Carlos Kaski, Attilio Maseri, Peter Collins, Petros Nihoyannopoulos, Philip A Poolewilson, Giuseppe M C RosanoAbstract:Objectives. Our aim was to study the clinical characteristics and evolution of symptoms and left ventricular function in a clinically homogeneous group of patients with Syndrome X (angina pectoris, positive eXercise test results and normal coronary arteriograms). Background. The Syndrome of angina with normal coronary arteriograms is heterogeneous and encompasses different pathogenetic entities. These characteristics may contribute to the eXisting controversy concerning the cause of Syndrome X. Methods. We studied 99 patients with Syndrome X (78 women, 21 men; mean age ± SD 48.5 ± 8 years). All underwent clinical characterization, ambulatory electrocardiographic (ECG) monitoring and echocardiographic assessment of left ventricular function during a follow-up period of 7 ± 4 years. Results. The Syndrome was more common in women than in men. Of the women, 61.5% were postmenopausal before the onset of chest pain. All 99 patients had eXertional angina, and 41 also had rest angina. The average duration of episodes of chest pain was > 10 min in 53% of patients. Sublingual nitrate was effective for relief of pain in 42% of patients. Transient ST segment depression was observed during ambulatory ECG monitoring in 64 patients and myocardial perfusion abnormalities in 22. During the first stage of the eXercise test, 32 patients had an increase > 20 mm Hg in systolic blood pressure and showed an earlier onset of ST depression and shorter eXercise time than did patients whose blood pressure increased ≤20%. During follow-up, no deaths or myocardial infarctions occurred, ventricular function was unchanged (shortening fraction 35.4 ± 4% vs. 35.6 ± 3%; heart failure developed in only one patient), systemic hypertension occurred in eight patients and conduction disturbances in four. Symptoms lessened in 11 patients, were variable or unchanged in 64 and worsened in 24. Conclusions. Syndrome X, as defined in this study, occurs predominantly in postmenopausal women. Patients usually have chest pain typical for angina, but conventional antianginal treatment is not often successful. Myocardial perfusion abnormalities occur in a small proportion of patients. Long-term survival is not adversely affected, and deterioration of cardiac function rarely occurs.
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comparison of regional myocardial blood flow in Syndrome X and one vessel coronary artery disease
American Journal of Cardiology, 1993Co-Authors: Alfredo R. Galassi, Juan Carlos Kaski, Filippo Crea, Luis I Araujo, Adriaan A Lammertsma, Giuseppe Pupita, Yusuke Yamamoto, Eldad Rechavia, Terry Jones, Attilio MaseriAbstract:Myocardial blood flow (MBF) was measured using continuous inhalation of oXygen-15-labeled carbon dioXide, and positron emission tomography before and after intravenous dipyridamole in 13 patients with Syndrome X (angina pectoris, angiographically normal coronary arteries, positive eXercise test and negative ergonovine test), 7 healthy subjects and 8 patients with 1-vessel coronary artery disease (CAD). In patients with Syndrome X, baseline MBF was greater than in healthy subjects and patients with CAO (1.24 ± 0.27 vs 0.87 ± 0.07 and 1.03 ± 0.23 ml/g/min, respectively; p < 0.05), and more heterogeneous (34 ± 7 vs 26 ± 5 and 25 ± 6, respectively; p < 0.05) as assessed by the coefficient of variation among myocardial regions ≤2.3 cm3. After dipyridamole, MBF in patients with Syndrome X was similar to that in healthy subjects (2.95 ± 0.75 vs 3.40 ± 0.82 ml/g/min; p = NS) and greater than in patients with CAD (1.78 ± 0.76 ml/g/min; p < 0.05). However in patients with both Syndrome X and CAD, MBF was more heterogeneous than in healthy subjects (48 ± 12 and 48 ± 11, respectively, vs 30 ± 7; p < 0.01). Thus, in patients with Syndrome X, MBF is abnormally heterogeneous both at baseline and after dipyridamole. These findings are compatible with the presence of dynamic alterations of small coronary arteries. Because these alterations appear to be very sparse within the myocardium, they can be undetected when myocardial perfusion, function and metabolism are assessed using conventional methods that are unable to detect small myocardial regions.
Dudley J Pennell - One of the best experts on this subject based on the ideXlab platform.
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abnormal subendocardial perfusion in cardiac Syndrome X detected by cardiovascular magnetic resonance imaging
The New England Journal of Medicine, 2002Co-Authors: Jonathan R Panting, Peter D Gatehouse, Guangzhong Yang, Frank Grothues, David N Firmin, Peter Collins, Dudley J PennellAbstract:A BSTRACT Background In cardiac Syndrome X (a Syndrome characterized by typical angina, abnormal eXercisetest results, and normal coronary arteries), conventional investigations have not found that chest pain is due to myocardial ischemia. Magnetic resonance techniques have higher resolution and therefore may be more sensitive. Methods We performed myocardial-perfusion cardiovascular magnetic resonance imaging in 20 patients with Syndrome X and 10 matched controls, both at rest and during an infusion of adenosine. Quantitative perfusion analysis was performed by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion indeX and the myocardial-perfusion reserve indeX (defined as the ratio of the myocardial perfusion indeX during stress to the indeX at rest). Results In the controls, the myocardial perfusion indeX increased in both myocardial layers with adenosine (in the subendocardium, from a mean [±SD] of 0.12±0.03 to 0.16±0.03 [P=0.02]; in the subepicardium, from 0.11±0.02 to 0.17±0.05 [P=0.002]); in patients with Syndrome X, the myocardial perfusion indeX did not change significantly in the subendocardium (0.13±0.02 vs. 0.14±0.03, P=0.11; P=0.09 as compared with controls) but increased in the subepicardium (from 0.11±0.02 to 0.20±0.04, P<0.001; P=0.11 for the comparison with controls). Adenosine provoked chest pain in 95 percent of patients with Syndrome X and 40 percent of controls (P<0.001). Conclusions In patients with Syndrome X, cardiovascular magnetic resonance imaging demonstrates subendocardial hypoperfusion during the intravenous administration of adenosine, which is associated with intense chest pain. These data support the notion that the chest pain may have an ischemic cause. (N Engl J Med 2002;346:1948-53.)
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abnormal subendocardial perfusion in cardiac Syndrome X detected by cardiovascular magnetic resonance imaging
The New England Journal of Medicine, 2002Co-Authors: Jonathan R Panting, Peter D Gatehouse, Guangzhong Yang, Frank Grothues, David N Firmin, Peter Collins, Dudley J PennellAbstract:Background In cardiac Syndrome X (a Syndrome characterized by typical angina, abnormal eXercise-test results, and normal coronary arteries), conventional investigations have not found that chest pain is due to myocardial ischemia. Magnetic resonance techniques have higher resolution and therefore may be more sensitive. Methods We performed myocardial-perfusion cardiovascular magnetic resonance imaging in 20 patients with Syndrome X and 10 matched controls, both at rest and during an infusion of adenosine. Quantitative perfusion analysis was performed by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion indeX and the myocardial-perfusion reserve indeX (defined as the ratio of the myocardial perfusion indeX during stress to the indeX at rest). Results In the controls, the myocardial perfusion indeX increased in both myocardial layers with adenosine (in the subendocardium, from a mean [±SD] of 0.12±0.03 to 0.16±0.03 [P=0.02]; in the subepicardium, from 0.11±0.02...
Attilio Maseri - One of the best experts on this subject based on the ideXlab platform.
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atenolol versus amlodipine versus isosorbide 5 mononitrate on anginal symptoms in Syndrome X
American Journal of Cardiology, 1999Co-Authors: Gaetano Antonio Lanza, Giuseppe Colonna, Vincenzo Pasceri, Attilio MaseriAbstract:: The effects of a beta blocker (atenolol), a calcium antagonist (amlodipine), and a nitrate (isosorbide-5-mononitrate) on anginal symptoms in 10 patients with Syndrome X were assessed in a crossover, double-blind, randomized trial. Only atenolol was found to significantly improve chest pain episodes, suggesting that it should be the preferred drug when starting pharmacologic treatment of patients with Syndrome X.
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cardiac Syndrome X clinical characteristics and left ventricular function long term follow up study
Journal of the American College of Cardiology, 1995Co-Authors: Juan Carlos Kaski, Attilio Maseri, Peter Collins, Petros Nihoyannopoulos, Philip A Poolewilson, Giuseppe M C RosanoAbstract:Objectives. Our aim was to study the clinical characteristics and evolution of symptoms and left ventricular function in a clinically homogeneous group of patients with Syndrome X (angina pectoris, positive eXercise test results and normal coronary arteriograms). Background. The Syndrome of angina with normal coronary arteriograms is heterogeneous and encompasses different pathogenetic entities. These characteristics may contribute to the eXisting controversy concerning the cause of Syndrome X. Methods. We studied 99 patients with Syndrome X (78 women, 21 men; mean age ± SD 48.5 ± 8 years). All underwent clinical characterization, ambulatory electrocardiographic (ECG) monitoring and echocardiographic assessment of left ventricular function during a follow-up period of 7 ± 4 years. Results. The Syndrome was more common in women than in men. Of the women, 61.5% were postmenopausal before the onset of chest pain. All 99 patients had eXertional angina, and 41 also had rest angina. The average duration of episodes of chest pain was > 10 min in 53% of patients. Sublingual nitrate was effective for relief of pain in 42% of patients. Transient ST segment depression was observed during ambulatory ECG monitoring in 64 patients and myocardial perfusion abnormalities in 22. During the first stage of the eXercise test, 32 patients had an increase > 20 mm Hg in systolic blood pressure and showed an earlier onset of ST depression and shorter eXercise time than did patients whose blood pressure increased ≤20%. During follow-up, no deaths or myocardial infarctions occurred, ventricular function was unchanged (shortening fraction 35.4 ± 4% vs. 35.6 ± 3%; heart failure developed in only one patient), systemic hypertension occurred in eight patients and conduction disturbances in four. Symptoms lessened in 11 patients, were variable or unchanged in 64 and worsened in 24. Conclusions. Syndrome X, as defined in this study, occurs predominantly in postmenopausal women. Patients usually have chest pain typical for angina, but conventional antianginal treatment is not often successful. Myocardial perfusion abnormalities occur in a small proportion of patients. Long-term survival is not adversely affected, and deterioration of cardiac function rarely occurs.
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comparison of regional myocardial blood flow in Syndrome X and one vessel coronary artery disease
American Journal of Cardiology, 1993Co-Authors: Alfredo R. Galassi, Juan Carlos Kaski, Filippo Crea, Luis I Araujo, Adriaan A Lammertsma, Giuseppe Pupita, Yusuke Yamamoto, Eldad Rechavia, Terry Jones, Attilio MaseriAbstract:Myocardial blood flow (MBF) was measured using continuous inhalation of oXygen-15-labeled carbon dioXide, and positron emission tomography before and after intravenous dipyridamole in 13 patients with Syndrome X (angina pectoris, angiographically normal coronary arteries, positive eXercise test and negative ergonovine test), 7 healthy subjects and 8 patients with 1-vessel coronary artery disease (CAD). In patients with Syndrome X, baseline MBF was greater than in healthy subjects and patients with CAO (1.24 ± 0.27 vs 0.87 ± 0.07 and 1.03 ± 0.23 ml/g/min, respectively; p < 0.05), and more heterogeneous (34 ± 7 vs 26 ± 5 and 25 ± 6, respectively; p < 0.05) as assessed by the coefficient of variation among myocardial regions ≤2.3 cm3. After dipyridamole, MBF in patients with Syndrome X was similar to that in healthy subjects (2.95 ± 0.75 vs 3.40 ± 0.82 ml/g/min; p = NS) and greater than in patients with CAD (1.78 ± 0.76 ml/g/min; p < 0.05). However in patients with both Syndrome X and CAD, MBF was more heterogeneous than in healthy subjects (48 ± 12 and 48 ± 11, respectively, vs 30 ± 7; p < 0.01). Thus, in patients with Syndrome X, MBF is abnormally heterogeneous both at baseline and after dipyridamole. These findings are compatible with the presence of dynamic alterations of small coronary arteries. Because these alterations appear to be very sparse within the myocardium, they can be undetected when myocardial perfusion, function and metabolism are assessed using conventional methods that are unable to detect small myocardial regions.
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epicardial coronary artery tone and reactivity in patients with normal coronary arteriograms and reduced coronary flow reserve Syndrome X
Journal of the American College of Cardiology, 1991Co-Authors: Juan Carlos Kaski, Wagner I Pereira, Eugene P Mcfadden, Dimitris Tousoulis, Alfredo R. Galassi, Filippo Crea, Attilio MaseriAbstract:The vasomotor response of proXimal and distal angiographically normal coronary artery segments was studied in 12 patients with Syndrome X, 17 age- and gender-matched patients with chronic stable angina and 10 control subjects with atypical chest pain and a normal coronary arteriogram. Ergonovine (300 fig by intravenous injection) and isosorbide dinitrate (1 mg by intracoronary injection) were administered to all patients. Computerized coronary artery diameter measurement (angiographically normal segments only) was carried out before and after the administration of ergonovine and nitrate. Baseline intraluminal diameters (mean ± SEM) of proXimal and distal coronary segments were not significantly different in control subjects and patients with Syndrome X or coronary artery disease (proXimal 2.88 ± 0.19,3.01 ± 0.13 and 2.86 ± 0.13 mm; distal 1.57 ± 0.09,1.70 ± 0.10 and 1.61 ± 0.06 mm, respectively). With ergonovine, proXimal segments constricted by 10 ± 2%, 7 ± 2% and 11 ± 3% and distal segments by 12 ± 3%, 14 ± 3% and 14 ± 2% in control subjects and patients with Syndrome X or coronary artery disease, respectively (p = NS). With isosorbide dinitrate, proXimal coronary segments dilated by 11 ± 2%, 10 ± 2% and 8 ± 2% (p = NS) and distal segments by 15 ± 2%, 11 ± 3% and 13 ± 2% (p = NS) in control subjects and patients with Syndrome X or coronary artery disease, respectively. Within groups, constriction in response to ergonovine and dilation in response to nitrate were not significantly different in proXimal and distal segments. The results of this study indicate that coronary diameters and the vasomotor response to ergonovine and isosorbide dinitrate of angiographically normal coronary artery segments at rest are not significantly different in patients with noncardiac chest pain, Syndrome X or coronary artery disease. Although coronary flow reserve is impaired in patients with Syndrome X, reactivity of large epicardial vessels to nitrate and ergonovine is within the physiologic range in these patients.
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mechanisms of angina pectoris in Syndrome X
Journal of the American College of Cardiology, 1991Co-Authors: Attilio Maseri, Juan Carlos Kaski, Filippo Crea, Tom CrakeAbstract:Syndrome X defines a group of patients who present with typical, usually eXertional angina pectoris and a normal coronary arteriogram. They often have a positive eXercise test, but direct signs of ischemia are detectable in only a minority of patients. A reduced coronary vasodilative response to dipyridamole or pacing is observed in such patients with or without a positive electrocardiographic eXercise test. It is proposed that patients with Syndrome X have a patchily distributed abnormal constriction of coronary prearteriolar vessels not involved in metabolic autoregulation of flow. An increased resistance of prearteriolar vessels can eXplain the reduced coronary vasodilative response observed in these patients, even when arterioles dilate maXimally. Distal to the most constricted arterioles a localized compensatory increase of adenosine concentration can cause angina even in the absence of ischemia because adenosine is an algogenic substance. Ischemia can develop when myocardial metabolic demand eXceeds blood supply or when metabolic or pharmacologic arteriolar vasodilation causes eXcessive reduction of pressure at the origin of the arterioles and possibly prearteriolar collapse. The more severe and confluent is the patchy prearteriolar constriction, the more detectable become the signs of myocardial ischemia. The proposed abnormal prearteriolar constriction could be caused by lack of endothelium-derived relaXing factor flow-mediated vasodilation, by abnormal nervous stimuli or by a combination of these two mechanisms. However, the causes of abnormal coronary prearteriolar constriction are not necessarily the same in all patients.
Jonathan R Panting - One of the best experts on this subject based on the ideXlab platform.
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abnormal subendocardial perfusion in cardiac Syndrome X detected by cardiovascular magnetic resonance imaging
The New England Journal of Medicine, 2002Co-Authors: Jonathan R Panting, Peter D Gatehouse, Guangzhong Yang, Frank Grothues, David N Firmin, Peter Collins, Dudley J PennellAbstract:A BSTRACT Background In cardiac Syndrome X (a Syndrome characterized by typical angina, abnormal eXercisetest results, and normal coronary arteries), conventional investigations have not found that chest pain is due to myocardial ischemia. Magnetic resonance techniques have higher resolution and therefore may be more sensitive. Methods We performed myocardial-perfusion cardiovascular magnetic resonance imaging in 20 patients with Syndrome X and 10 matched controls, both at rest and during an infusion of adenosine. Quantitative perfusion analysis was performed by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion indeX and the myocardial-perfusion reserve indeX (defined as the ratio of the myocardial perfusion indeX during stress to the indeX at rest). Results In the controls, the myocardial perfusion indeX increased in both myocardial layers with adenosine (in the subendocardium, from a mean [±SD] of 0.12±0.03 to 0.16±0.03 [P=0.02]; in the subepicardium, from 0.11±0.02 to 0.17±0.05 [P=0.002]); in patients with Syndrome X, the myocardial perfusion indeX did not change significantly in the subendocardium (0.13±0.02 vs. 0.14±0.03, P=0.11; P=0.09 as compared with controls) but increased in the subepicardium (from 0.11±0.02 to 0.20±0.04, P<0.001; P=0.11 for the comparison with controls). Adenosine provoked chest pain in 95 percent of patients with Syndrome X and 40 percent of controls (P<0.001). Conclusions In patients with Syndrome X, cardiovascular magnetic resonance imaging demonstrates subendocardial hypoperfusion during the intravenous administration of adenosine, which is associated with intense chest pain. These data support the notion that the chest pain may have an ischemic cause. (N Engl J Med 2002;346:1948-53.)
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abnormal subendocardial perfusion in cardiac Syndrome X detected by cardiovascular magnetic resonance imaging
The New England Journal of Medicine, 2002Co-Authors: Jonathan R Panting, Peter D Gatehouse, Guangzhong Yang, Frank Grothues, David N Firmin, Peter Collins, Dudley J PennellAbstract:Background In cardiac Syndrome X (a Syndrome characterized by typical angina, abnormal eXercise-test results, and normal coronary arteries), conventional investigations have not found that chest pain is due to myocardial ischemia. Magnetic resonance techniques have higher resolution and therefore may be more sensitive. Methods We performed myocardial-perfusion cardiovascular magnetic resonance imaging in 20 patients with Syndrome X and 10 matched controls, both at rest and during an infusion of adenosine. Quantitative perfusion analysis was performed by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion indeX and the myocardial-perfusion reserve indeX (defined as the ratio of the myocardial perfusion indeX during stress to the indeX at rest). Results In the controls, the myocardial perfusion indeX increased in both myocardial layers with adenosine (in the subendocardium, from a mean [±SD] of 0.12±0.03 to 0.16±0.03 [P=0.02]; in the subepicardium, from 0.11±0.02...
