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PubMed2003

Cardiological syndrome X. Non-invasive assessment of endothelial function and arterial compliance.

BACKGROUND: Mechanisms responsible for cardiological syndrome X are complex and not well understood. It has been postulated that impaired endothelial function and abnormal reactivity of coronary vessels may play a role in the pathogenesis of this condition. AIM: To assess mechanical properties of peripheral arterial vessels and both endothelium-dependent and endothelium-independent vessel reactivity in patients with or without atherosclerotic lesions in coronary arteries. METHODS: The study group consisted of 100 patients with typical angina and positive exercise test who underwent coronary angiography. Based on angiographic results, the patients were divided into two groups: 50 patients with normal coronary angiograms and 50 age- and gender-matched patients with at least one significant coronary artery lesion (coronary artery disease (CAD) group). The control group consisted of 40 healthy volunteers without risk factors of atherosclerosis. The compliance of arterial vessels was assessed by automatic measurement of pulse wave velocity (PWV). Endothelial function was examined by ultrasonographic measurement of the diameter of brachial artery following passive hyperaemia (endothelium-dependent vessel distension) and following nitroglycerine (endothelium-independent mechanism). RESULTS: Among all three studied groups, the PWV values were the highest in patients with CAD. Patients with syndrome X had significantly higher PWV than in controls. A cut-off PWV value of 10.5 m/s distinguished patients with syndrome X from those with CAD. Endothelium-dependent arterial distensibility was significantly lower in patients with syndrome X than in controls; the lowest values were observed in patients with CAD. Among patients with syndrome X, the endothelium-dependent arterial vessel distensibility was the only parameter significantly influencing PWV results. CONCLUSIONS: PWV was significantly increased in patients with syndrome X which suggests a decreased arterial vessel compliance. These results and the impairment of endothelium-dependent relaxation suggest a similar pathomechanism of altered arterial reactivity in patients with syndrome X and in patients with CAD.

Adult↗
PubMed1998

Therapeutic benefits of cilazapril in patients with syndrome X.

OBJECTIVES: Although the pathophysiology of syndrome X (angina pectoris, positive ECG test findings and normal coronary arteriogram) is unclear, it is generally accepted that intracellular metabolic changes resulting from abnormal constriction of prearteriolar vessels due to endothelium-dependent vasodilation abnormalities may play a role in the pathogenesis. We established the effect of long-term treatment with cilazapril, an angiotensin-converting enzyme inhibitor, which prevents the effect of angiotensin II in the tonic control of vascular resistance. METHODS: 18 patients (15 women and 3 men, mean age 43.2 +/- 4.6 years) with syndrome X were included in this study. A randomized double-blind crossover placebo-controlled trial was done. After a 1-week washout period, patients received either cilazapril 2 x 2.5 mg or placebo for 3 weeks, followed by 3 weeks of the other therapy. At the end of two periods, an exercise ECG test (modified Bruce protocol) was employed. RESULTS: The magnitude of ST segment depression was significantly decreased during treatment with cilazapril compared with placebo. On the other hand, total exercise time and time to 1 mm ST segment depression were significantly prolonged by cilazapril. However, rate pressure products were not significantly different at peak exercise at or at 1 mm of ST segment depression during both therapies. CONCLUSION: Cilazapril exerted a beneficial therapeutic effect in cases with syndrome X. The possible mechanism of this effect may be a modulation of coronary tone at the microcirculation level.

Adult↗
PubMed1994

Unusual forms of ischemic heart disease.

Unusual forms and causes of ischemic heart disease include angina pectoris in the presence of normal coronary arteries (syndrome X), congenital coronary abnormalities, vasculitic disorders, and graft atherosclerosis after cardiac transplantation. There is now evidence that endothelial dysfunction of coronary resistance vessels can account for abnormalities of the coronary microvasculature and possibly, myocardial ischemia and chest pain. The incidence of syndrome X appears to be higher in women, particularly those who have undergone hysterectomy. An intriguing hypothesis is that low estrogen levels may be associated with reduced expression of nitric oxide (reflecting endothelial dysfunction). The presence of coronary abnormalities in the young should not be underestimated. Syncope and arrhythmias are observed frequently in this patient population and warrant vigorous exploration. Worldwide, cardiac transplantation is now carried out in approximately 4500 patients yearly, with excellent (80% to 90%) 1-year survival due to improved immunosuppression. However, accelerated atherosclerosis develops rapidly postoperatively and is the main cause of late death. The link between cellular rejection of the myocardium and transplant coronary artery disease is not clear. The process of transplant coronary artery disease is believed to be due to chronic immune injury followed by intimal smooth-muscle proliferation and lipid deposition in the vascular wall. By the time it is detected by coronary angiography, the disease is far advanced and not susceptible to routine revascularization procedures. A prospective, randomized study of diltiazem versus no calcium blocker started early after transplantation has documented highly significant reductions in transplant atherosclerosis as measured by lumen narrowing, clinical events, and rates of retransplantation or death due to the process.(ABSTRACT TRUNCATED AT 250 WORDS)

Death, Sudden, Cardiac↗
PubMed2005

Role of endothelial dysfunction and insulin resistance in angina pectoris and normal coronary angiogram.

Angina pectoris and a normal coronary angiogram or cardiac syndrome X is a heterogeneous syndrome that probably encompasses different pathophysiological entities. Patients affected by cardiac syndrome X are often women presenting with severe, invalidating chest pain. However, there is a significant discrepancy among the severity of symptoms, the lack of hemodynamic evidence of myocardial ischemia and the relatively benign long-term prognosis. The vascular endothelium has numerous important functions, including the regulation of vascular tone, blood flow and permeability, secreting both vasorelaxing and vasoconstricting factors. It has been found that both endothelium and non-endothelium-mediated coronary blood flow are impaired in patients with cardiac syndrome X. Interestingly, it has been shown that impaired nitric oxide-dependent vasodilation could increase coronary microvessel tone and produce spasm. It has also been reported that circulating endothelin-1 levels are elevated with a direct relationship between endothelin-1 levels and impaired coronary flow reserve in these patients. In addition, patients with high endothelin-1 levels showed a time onset of chest pain during exercise significantly lower compared to patients with low endothelin-1 concentrations. Moreover, the nitric oxide/endothelin-1 ratio was found decreased in patients with cardiac syndrome X and endothelin-1 levels were also positively correlated with fasting asymmetric dimethylarginine levels. All in all, these data suggest a role of endothelial dysfunction as a cause of regional myocardial and peripheral blood flow abnormalities. Further studies are necessary to characterize the prevailing mechanisms determining alterations in nitric oxide/endothelin-1 pathway in these patients, in order to find new therapies able to improve both quality of life and prognosis.

Animals↗
PubMed1997

Abnormal cardiac adrenergic nerve function in patients with syndrome X detected by [123I]metaiodobenzylguanidine myocardial scintigraphy.

BACKGROUND: Previous studies have suggested that an abnormal cardiac adrenergic tone may have a pathophysiological role in syndrome X (effort angina, positive exercise testing, angiographically normal coronary arteries). METHODS AND RESULTS: To evaluate cardiac adrenergic nerve function, we performed [123I]metaiodobenzylguanidine (MIBG) myocardial scintigraphy in 12 patients with syndrome X and 10 control subjects. Cardiac MIBG uptake was assessed by the heart/mediastinum (H/M) ratio and by an MIBG uptake defect score (higher values=lower uptake). In syndrome X patients, we also correlated MIBG scintigraphic findings with stress myocardial perfusion as assessed by 201Tl scintigraphy. An inferior MIBG defect was observed in only 1 control subject, whereas 9 patients (P<.01) showed MIBG defects. The heart was totally or almost totally invisible on MIBG images in 5 patients, and predominantly regional defects were observed in 4. The H/M ratio was lower (1.70+/-0.6 versus 2.2+/-0.3, P=.03) and MIBG uptake defect score higher (35+/-31 versus 4+/-2, P=.003) in syndrome X patients. Reversible stress thallium perfusion defects were found in 62% of patients with MIBG defects but in no patient with normal MIBG uptake. MIBG defects persisted unchanged in 7 patients at a 5+/-3-month follow-up study. CONCLUSIONS: In this study, obvious defects in global and/or regional cardiac MIBG uptake, indicating an abnormal cardiac adrenergic nerve function, were detected in 75% of patients with syndrome X. These findings strongly support the cardiac origin of chest pain in syndrome X, although the mechanisms and the pathophysiological meaning of the abnormal cardiac MIBG uptake in these patients deserve further investigation.

3-Iodobenzylguanidine↗
PubMed2006

Myocardial perfusion quantification in patients suspected of cardiac syndrome X with positive and negative exercise testing: a [13N]ammonia positron emission tomography study.

BACKGROUND: The combination of angina pectoris, angiographically normal coronary arteries, and a positive exercise stress test (EST) is referred to as cardiac syndrome X. However, a large group of patients suspected of syndrome X reveals a normal exercise stress test and weakens the diagnosis of syndrome X. Previous studies demonstrated an impaired coronary flow reserve on ammonia positron emission tomography (PET) in patients with syndrome X. AIM: To evaluate the coronary flow reserve in patients suspected of syndrome X with positive and negative EST findings, using [(13)N]ammonia PET as the diagnostic aid. METHODS: Forty-two patients with chest pain and a normal coronary angiography, were analysed by exercise stress testing (EST) and the dypyridamole stress test (DST) on [(13)N]ammonia PET. Two subgroups were predefined, based on outcome of EST: an EST positive and negative group. A normal control group was used as the reference method. RESULTS: A total of 24 (57%) out of 42 patients had significant ST-T changes (EST positive). [(13)N]ammonia PET showed a significantly lower rest flow in the EST positive and EST negative group compared to controls (P<0.001 and P=0.0028, respectively). DST [(13)N]ammonia PET perfusion was significantly reduced in flow in both the EST positive and EST negative groups (P<0.001 both), as was the DST/rest [(13)N]ammonia perfusion reserve (P<0.001 for both), compared to normal controls. CONCLUSION: PET demonstrates a reduced coronary flow reserve in patients suspected of syndrome X, irrespective of the EST findings.

Adult↗
PubMed1994

Abnormal autonomic control of the cardiovascular system in syndrome X.

Anomalies of autonomic control of the coronary circulation may play a role in the development of syndrome X (angina pectoris, ischemic-appearing results on exercise test, and normal coronary arteriograms). Twenty-six patients with syndrome X and 20 healthy sex- and age-matched control subjects were studied by means of analysis of heart rate variability during 24-hour Holter monitoring. Spectral and nonspectral parameters of heart rate variability were investigated. Mean heart rate was similar in patients with syndrome X and in control subjects. Patients with syndrome X had significantly lower standard deviation of all normal RR intervals, a lower percentage of adjacent normal RR intervals > 50 ms in difference (126.4 +/- 22 vs 149 +/- 43 ms, p < 0.05; 6.3 +/- 4 vs 11.2 +/- 7%, p < 0.05; respectively), and a trend toward lower values of time-domain parameters. Lower values of total power and low frequency were also observed in patients with syndrome X (1273 +/- 693 vs 1790 +/- 989 ms2, p < 0.05; 406 +/- 176 vs 729 +/- 455 ms2, p < 0.01, respectively). An inverse correlation between heart rate and measures of heart rate variability was found in syndrome X but not in control subjects. High- and low-frequency power showed a similar circadian pattern in syndrome X patients and control subjects. Patients and control subjects were then allocated into 2 groups according to the median RR duration: syndrome X1 and control 1 with high mean heart rate, and syndrome X2 and control 2 with low mean heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2001

Evidence of parasympathetic impairment in some patients with cardiac syndrome X.

OBJECTIVES: Cardiac syndrome X (SX) is a clinical condition characterised by angina, positive exercise stress test and negative coronary angiography; it has often been attributed to sympathetic hyperactivity. Here we tested the hypothesis that a parasympathetic, rather than a sympathetic, dysfunction could be the cause of the autonomic imbalance observed in SX. METHODS: In 20 subjects with diagnosed SX and in 12 age-matched controls, we studied autonomic function by performing spectral analysis of RR interval and finger arterial pressure (SAP), in supine position and during head-up tilting. We also carried out a set of tests of parasympathetic function. RESULTS: The group of SX patients did not differ significantly from control subjects in any of the variables tested. In a subgroup of 13 SX, however, tilting increased the low-frequency power of SAP, but did not induce the expected increase in low-frequency and decrease in high-frequency power of RR. These patients, in supine position, had significantly lower sinus arrhythmia and a higher ratio of low to high frequency of RR, in comparison with control subjects. We interpreted these differences as signs of reduced parasympathetic, but essentially normal sympathetic, activity. The parasympathetic tests confirmed vagal impairment in the same SX subjects. On the other hand, all the tests indicated normal parasympathetic functions in the control subjects and in those SX patients who displayed the expected spectral changes in tilting. CONCLUSIONS: In about two thirds of the patients with SX, the pathophysiological mechanism causing the symptoms could be related to the reduced parasympathetic tone, rather than to an augmented sympathetic activity.

Analysis of Variance↗
PubMed1997

Myocardial insulin resistance in patients with syndrome X.

Insulin resistance is common in patients with angina pectoris, a positive exercise electrocardiogram, and normal coronary angiograms (syndrome X). It is still not known whether insulin resistance affects the cardiac muscle itself and, if so, whether insulin resistance involves myocardial hemodynamics and energy metabolism. We investigated hemodynamics as well as metabolite exchanges across the heart and the forearm in eight patients with syndrome X and eight control subjects during a baseline period after an overnight fast and during a hyperinsulinemic-euglycemic clamp. Myocardial hemodynamics and metabolism were studied at rest, during pace stress, and in the recovery period after pacing. Neither coronary sinus blood flow nor forearm blood flow differed between the groups before and during the clamp. Whole body insulin-stimulated glucose uptake was decreased in the patients (15.6+/-2.1 vs. 23.1+/-2.0 micromol x kg-1 x min-1). Insulin-stimulated glucose uptake in the forearm and the cardiac muscle was equally reduced in the patients (46+/-5 and 48+/-5%). Myocardial glucose uptake correlated with total arterial delivery in the control subjects (r = 0.63, P < 0.01), but not in patients (r = 0.22, P = 0.13). Carbohydrate and lipid oxidation was similar in the two groups at rest, and changes during the clamp were not different in control subjects and patients either at rest, during pacing, or in the recovery period. Patients with syndrome X exhibit myocardial insulin resistance, but cardiac energy metabolism remains unaffected. In patients with syndrome X, insulin-stimulated glucose uptake is independent from myocardial blood flow.

Blood Glucose↗
PubMed1997

Abnormal myocardial glucose handling in patients with syndrome X: effect of beta-adrenergic blockade.

The present study was designed to test the hypothesis that patients with angina, positive exercise test and angiographically smooth coronary arteries (syndrome X), may exhibit abnormal myocardial glucose handling, as assessed by fluorodeoxyglucose (FDG) and positron emission tomography (PET) and to investigate the possibility that this abnormality could be reversed by treatment with betablockers, the drugs of choice in most patients with syndrome X. Eight consecutive patients (4 females, age 53 +/- 4 yrs) with syndrome X were studied. Off therapy, they underwent stress/rest 99m-TcMIBI SPET (360 degrees) and assessment of resting glucose metabolism by PET. PET studies were again performed after a 10 day treatment period on oral atenolol (100 mg/o.d.). All patients exhibited significant fasting FDG uptake in 2 or more myocardial regions. Overall, there were 28 of 48 segments (58%) with abnormal tracer uptake. On atenolol, there were only 5 segments with persistent FDG uptake (10%) in 2 patients. At rest, 7 patients exhibited perfusion defects in 14 myocardial segments. With stress performed in pharmacological wash-out, 5 patients developed perfusion defects in 10 myocardial segments. Eight of these segments were already underperfused at rest, and showed further reduction in perfusion after stress. All hypoperfused segments showed abnormal FDG uptake when the PET study was performed off therapy. The results suggest that, in patients with syndrome X, imbalance of the demand/supply ratio, either caused by limited coronary flow reserve or by primary vasoconstriction with reduction in myocardial perfusion, may determine a sustained metabolic shift towards anaerobic glycolysis. The mechanism by which atenolol improves metabolism in these patients could be simply related to reduction in O2 consumption.

Adrenergic beta-Antagonists↗
PubMed2002

Abnormal subendocardial perfusion in cardiac syndrome X detected by cardiovascular magnetic resonance imaging.

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 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.

Adenosine↗
PubMedDate not supplied

Esterified estrogens combined with methyltestosterone improve emotional well-being in postmenopausal women with chest pain and normal coronary angiograms.

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 17beta-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.

Adult↗
PubMed1998

Comparison of coronary endothelial dynamics with electrocardiographic and left ventricular contractile responses to stress in the absence of coronary artery disease.

Coronary artery endothelial dysfunction has been proposed as a cause of myocardial ischemia and symptoms in patients with angina-like chest pain despite normal coronary angiograms, especially those with ischemic-appearing ST-segment depression during exercise (syndrome X). We measured coronary vasomotor responses to acetylcholine (3 to 300 microg/min) in 42 patients (27 women and 15 men) with effort chest pain and normal coronary angiograms who also had normal electrocardiograms and echocardiograms at rest. All patients underwent treadmill exercise testing and measurement of systolic wall thickening responses to dobutamine (40 microg/kg/min) during transesophageal echocardiography. There were no differences in the acetylcholine-stimulated epicardial coronary diameter (+5+/-13% vs +1+/-13%, p=0.386) and flow (+179+/-90% vs +169+/-96%, p=0.756), or in the systolic wall thickening responses (+134+/-65% vs +118+/-57%, p=0.445) from baseline values in the 12 syndrome X patients compared with the 30 patients with negative exercise test results. In patients in the lowest quartile of coronary flow responses to acetylcholine, dobutamine increased systolic wall thickening by 121+/-73%; 3 had ischemic-appearing ST-segment depression during this stress. This contractile response to dobutamine was no different than the increase in systolic wall thickening (129+/-48%, p=0.777) in patients in the highest quartile of coronary flow responses, 3 of whom also had ischemic-appearing ST-segment depression during this stress. Thus, coronary endothelial dysfunction in the absence of coronary artery disease does not account for ischemic-appearing ST-segment depression in patients with chest pain despite normal coronary angiograms. Further, coronary endothelial dysfunction is not associated with myocardial contractile responses to stress consistent with myocardial ischemia.

Acetylcholine↗
PubMed1993

Left ventricular hypercontractility and ST segment depression in patients with syndrome X.

OBJECTIVES: This study was designed to assess the relation between rest left ventricular function and exercise capacity in patients with syndrome X. BACKGROUND: Clinical observation has suggested that some patients with syndrome X have a high rest left ventricular ejection fraction. In this study we determined the relation between left ventricular ejection fraction and exercise capacity and the electrocardiographic (ECG) changes that develop on exercise. METHODS: The pattern of left ventricular function, exercise capacity and 24-h ambulatory ECG monitoring were studied in 37 patients (9 men, 28 women; mean age 52 +/- 7 years) with syndrome X (angina with normal coronary arteries and a positive exercise test result). All patients had normal findings on echocardiogram and rest ECG. All treatment was discontinued for > or = 48 h. Left ventricular ejection fraction was determined by computerized analysis of the left ventricular angiogram. In patients with syndrome X, exercise duration and heart rate were measured at 1-mm ST segment depression and at peak exercise. RESULTS: Left ventricular hypercontractility (ejection fraction > or = 80%) was observed in 12 patients (32%) (group 1), whereas 25 patients (68%) had normal left ventricular contraction (group 2). The time to 1-mm ST depression on exercise testing was significantly earlier in group 1 than in group 2 (5.13 +/- 1.03 vs. 10.76 +/- 0.63 min, respectively, p < 0.001). The magnitude of the ST segment depression at peak exercise was significantly greater in group 1 than in group 2 (2.03 +/- 0.2 vs. 1.33 +/- 0.05 mm, respectively, p < 0.001). The mean time for ST segment depression to normalize was significantly greater in group 1 than in group 2 (4.76 +/- 0.78 vs. 3.16 +/- 0.39 min, respectively, p < 0.05). Linear regression analysis of all patients with syndrome X showed a significant correlation between exercise duration and ejection fraction (r = 0.55, p < 0.001). The mean circadian variation of heart rate and episodes of ST segment depression on 24-h ambulatory ECG monitoring were similar in the two groups of patients. CONCLUSIONS: These findings indicate that approximately one third of patients with chest pain, normal coronary angiograms and a positive exercise test have left ventricular hypercontractility, and this is associated with the development of ST segment depression at a lower heart rate and work load and a longer time to normalization of ST segment depression after exercise.

Adult↗
PubMed1996

Insulin sensitivity in cardiological syndrome X.

OBJECTIVES: To test whether cardiological syndrome X is an insulin-resistant state. SETTING, DESIGN AND SUBJECTS: The coronary care unit of a referral centre for angina pectoris in Pisa, Italy. A case-control study, involving 10 patients with unequivocal (angiographycally proven) cardiological syndrome X, but normal glucose tolerance, blood pressure and lipid levels, and 13 matched healthy subjects. MAIN OUTCOME MEASURES: Insulin sensitivity and pattern of substrate oxidation (assessed by the euglycaemic insulin clamp technique in combination with indirect calorimetry). RESULTS: Fasting plasma glucose and insulin levels were 5.05 +/- 0.11 versus 4.88 +/- 0.11 mmol l-1 and 68 +/- 10 versus 56 +/- 6 pmol l-1, respectively (controls versus patients, ns). During the insulin clamp, glucose disposal rate was nearly identical in patients and controls (25.9 +/- 1.8 and 27.2 +/- 1.8 mumol kg-1 min-1, respectively. P = 0.88). Non-oxidative glucose disposal accounted for similar proportions of total glucose uptake (59 versus 53%, patients versus controls, ns). Resting energy expenditure (13.7 +/- 0.6 versus 13.8 +/- 0.8 cal kg-1 min-1, ns) and insulin-induced thermogenesis were similar in the two groups. Fasting plasma NEFA concentrations (0.64 +/- 0.09 and 0.64 +/- 0.06 mmol l-1, patients and controls, ns) fell in a similar time-course and to virtually identical nadirs (0.13 +/- 0.02 and 0.14 +/- 0.02 mmol l-1) after insulin infusion. Fasting plasma potassium was similar in patients and controls (3.99 +/- 0.10 and 4.16 +/- 0.04 mmol l-1, ns), and insulin induced equivalent hypokalaemia (-14 versus -19%). CONCLUSIONS: None of the in vivo actions of insulin were impaired in patients with 'pure' syndrome X when compared to matched controls. Therefore, we conclude that cardiological syndrome X is not an insulin resistant state per se, and that any decrease in insulin sensitivity found in this condition is likely to be secondary.

Blood Glucose↗
PubMed1999

Reduced vasodilator capacity in syndrome X related to structure and function of resistance arteries.

The combination of angina pectoris, angiographically normal epicardial coronary arteries, and a positive exercise test is referred to as syndrome X. Previous studies have demonstrated an impaired coronary flow reserve and a peripheral vascular dysfunction, suggesting that vascular abnormalities in syndrome X may not be confined to the heart. The aim of this study was to investigate whether any vascular disorder of syndrome X is due to intrinsic structural or functional disturbances in resistance arteries. We compared 16 patients with syndrome X (56.6+/-1.2 years, 3 men) with 15 matched control subjects. Myocardial blood flow was measured with 13N-ammonia positron emission tomography. Forearm blood flow was measured in the brachial artery with high-resolution ultrasound. Gluteal subcutaneous resistance arteries were dissected and mounted on a myograph for measurement of active tension development, lumen diameter, and media thickness. Baseline myocardial blood flow was similar in patients and controls, but dipyridamole-induced hyperemia was decreased in patients (1.67+/-0.13 vs 2.31+/-0.12 ml/ min/g, p <0.01). Patients and controls had similar baseline forearm blood flow, but hyperemic flow after transient occlusion of the brachial artery was impaired in patients (198+/-20 vs 273+/-32 ml/min, p <0.05). Isolated resistance arteries showed no differences in constriction to noradrenaline, or relaxation to acetylcholine, dipyridamole, or nitroglycerin. Furthermore, the ratio between media thickness and lumen diameter were similar in syndrome X patients and controls. Our data show that when compared with a well-matched control group, syndrome X patients have a decreased coronary and peripheral vasodilator capacity. However, this is not reflected by functional abnormalities or structural changes as evaluated in subcutaneous resistance arteries. We conclude that syndrome X is not a generalized intrinsic abnormality of the resistance circulation.

Arteries↗
PubMed1996

Transient autonomic dysfunction precedes ST-segment depression in patients with syndrome X.

Increased sympathetic drive has been suggested to play a role in the pathogenesis of syndrome X (angina pectoris, positive exercise testing, and angiographically normal coronary arteries). Heart rate variability (HRV) studies have shown that patients with syndrome X have an imbalance in autonomic nervous system activity (sympathetic predominance). However, it is not known if transient ST-segment depression which occurs in syndrome X during daily activities is related to this autonomic nervous system dysfunction. This study investigates the relation between the response of the autonomic nervous system, as assessed by HRV analysis, and the occurrence of transient ST-segment depression during 24-hour ambulatory electrocardiographic monitoring in 23 patients (4 men and 19 women, mean age 55 +/- 6 years) with syndrome X. The frequency-domain variables of HRV low-frequency (0.04 to 0.15 Hz) and high-frequency (0.15 to 0.40 Hz) power were measured at 6-minute intervals during the 30 minutes preceding the onset of transient ST-segment depression. Fourteen patients (61%) had > or = 1 episode of ST-segment depression in the 24 hours, whereas the remaining 9 patients (39%) had no significant ST-segment change. HRV measures differed according to whether or not ST-segment depression was associated with increased heart rate. Episodes of ST-segment depression associated with increased heart rate were preceded by a reduction of high-frequency power and an increase in the low-frequency--high-frequency ratio, whereas episodes of ST-segment depression not associated with increased heart rate showed no significant HRV changes. Low-frequency power remained unchanged irrespective of heart rate. Thus, in patients with syndrome X, a sympathovagal imbalance (sympathetic predominance due to vagal tone withdrawal) precedes episodes of ST-segment depression that are associated with an increased heart rate.

Autonomic Nervous System↗
PubMed1999

Enhanced exercise-induced hyperkalemia in patients with syndrome X.

OBJECTIVES: The purpose of this study was to determine whether patients with syndrome X have altered potassium metabolism. BACKGROUND: Patients with syndrome X have angina pectoris and exercise induced ST segment depression on the electrocardiogram despite normal coronary angiograms. Increasing evidence suggests that myocardial ischemia is uncommon in these patients. Altered potassium metabolism causing interstitial potassium accumulation in the myocardium may be an alternative mechanism for chest pain and ST segment depression in syndrome X. METHODS: We compared the magnitude of exercise-induced hyperkalemia in 16 patients with syndrome X (12 female and four male, mean +/- SD age 53 +/- 6 years) and 15 matched healthy control subjects. The participants underwent a bicycle test at a fixed load of 75 W for 10 min, and blood samples were taken for analysis of potassium, catecholamines and lactate before, during and in the recovery period after exercise. In five patients with syndrome X, the test was repeated during alpha1 adrenoceptor blockade. RESULTS: Baseline concentrations of serum potassium, plasma catecholamines and plasma lactate were similar in patients and control subjects. The rate of exercise-induced increment of serum potassium was increased in the patients (70 +/- 29 vs. 30 +/- 21 micromol/liter/min in control subjects, p < 0.001). Six patients, who stopped before 10 min of exercise, showed very rapid increments in serum potassium concentration. Compared to the control subjects, patients also demonstrated larger increments in rate-pressure product, plasma norepinephrine and lactate concentrations during exercise. The rate of serum potassium increment correlated with the rate of plasma norepinephrine increment in the patients (r = 0.63, p < 0.02), but not in the control subjects (r = 0.01, p = 0.97). Blockade of alpha1 adrenoceptors decreased systolic blood pressure at baseline, but did not influence the increment of serum potassium, plasma catecholamines and lactate. CONCLUSIONS: Patients with syndrome X have enhanced exercise induced hyperkalemia in parallel with augmented increases of circulating norepinephrine and lactate. The prevailing mechanisms behind the abnormal potassium handling comprise sources distinct from alpha1-adrenoceptor activation.

Exercise Test↗