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PubMed1994

Southwestern Internal Medicine Conference: the syndrome of angina pectoris: role of visceral pain perception.

Angina pectoris is a pain syndrome caused by coronary arteriosclerosis but also by a number of other disorders, including microvascular angina, gastroesophageal reflux (GER), and esophageal dysmotility. The relationship between abnormal physiology and pain in these conditions is complex. Simultaneous ambulatory monitoring of esophageal pH and motility has demonstrated that patients may have identical episodes of chest pain with acid reflux, dysmotility, both types of events, or neither. Patients may have anginal chest pain with inflation of an esophageal balloon, and patients with microvascular angina may have pain with catheter manipulation in the right atrium. Recent evidence suggests that disorders of visceral pain perception may play a role in both chest pain of esophageal origin and microvascular angina. The physiology of visceral pain is reviewed, including concepts of convergence of somatic and visceral afferent input, descending modulation of pain perception, and sensitization of visceral pain afferents. An approach to evaluation and treatment of chest pain in patients with angiographically normal coronary arteries is outlined.

Angina Pectoris↗
PubMed2003

Relation between the timing of the last preinfarction angina and microvascular reperfusion in patients with recanalized acute myocardial infarction.

In patients with recanalized acute myocardial infarction (AMI), the relation between the timing of preinfarction angina (PA) and microvascular reperfusion remains unclear. A total of 186 patients (114 with anterior and 72 with inferior AMI) who had total occlusion and TIMI 3 recanalization < or = 6 hours from the onset of AMI were divided into 4 groups according to the time interval between the last episode of PA and the onset of AMI: < or = 2 hours (group A, n = 52); 2 to 48 hours (group B, n = 43), > or = 48 hours (group C, n = 33), and no PA (group D, n = 58). The angiographic myocardial blush grade, a marker of microvascular reperfusion, was retrospectively assessed immediately after recanalization. There were no differences in baseline characteristics, except for sex among the 4 groups. Myocardial blush grade 3 was more frequent (42% vs 21%, 9%, and 14%) and peak creatine kinase was lower (2659 vs 3455, 4422, and 4622 mU/mL) in group A than in groups B, C, and D (all P < 0.05). Multivariate analysis showed that PA occurring < or = 2 hours before AMI (OR 3.88, P < 0.05), a smaller summed ST-segment elevation before recanalization (OR 0.84, P < 0.01), earlier time to recanalization (OR 0.52, P < 0.05), and interior AMI (OR 4.87, P < 0.05) were independently associated with adequate microvascular reperfusion. We conclude that PA < or = 2 hours before the onset of AMI is independently associated with adequate microvascular reperfusion after recanalization in patients with AMI.

Adult↗
PubMed2006

The incidence of gastro-esophageal disease for the patients with typical chest pain and a normal coronary angiogram.

BACKGROUND: Although patients may present with typical chest pain and exhibit ischemic changes on the cardiac stress test, they are frequently found to have a normal coronary angiogram. Thus, we wanted to determine which procedures should be performed in order to make an adequate diagnosis of the cause of chest pain. METHODS: 121 patients (males: 42, 34.7%) who had a normal coronary angiogram with typical chest pain were included in this study. All the patients underwent upper endoscopy, Bernstein's test and esophageal manometry. RESULTS: Among the 121 patients, clinically stable angina was noted in 107 (88.4%). Stress testing was done in 82 (67.8%); it was positive in 52 (63.4%). Endoscopic findings were erosive gastritis in 18 (14.8%), gastric ulcer in 4 (3.3%), duodenal ulcer in 5 (4.1%), and reflux esophagitis in 16 (13.2%). Positive results were observed on Berstein's test for 68 patients (56.2%); 59 (86.8%) of them had non-erosive reflux disease. On the esophageal manometry, 35 (28.9%) of these patients had motility disorders. Nutcracker esophagus was observed in 27 patients (22.3%), nonspecific esophageal motility disorder was observed in 5 (4.1%), and hypertensive lower esophageal sphincter was observed in 3 (2.5%). Among the 52 patients with positive cardiac stress testing and a negative coronary angiogram (this clinically corresponded to microvascular angina), 46 patients (85.1%) showed abnormal findings on the gastro-esophageal studies. CONCLUSIONS: In our study, 85.1% of the patients with microvascular angina revealed positive results of gastric or esophageal disease. In spite of any existing evidence of microvascular angina or cardiac syndrome X, it would be more advisable to perform gastro-esophageal studies to adequately manage chest pain.

Adult↗
PubMed2000

[Two cases of microvascular vasospastic angina usefulness of 99mTc-tetrofosmin myocardial SPECT in clinical diagnosis].

Case 1 involved a 52-year-old man with angina chest pain at rest and case 2 involved a 63-year-old woman with chest oppression at rest. An electrocardiogram (ECG) showed negative T wave in III and aVF leads in case 1, and complete atrioventricular block and ST segment depression in II, III, aVF, and V5-6 leads in case 2. In both cases, 99mTc-tetrofosmin myocardial SPECT showed reduced uptake in the inferior and posterior wall. Although bath patients' left coronary arteriographies were normal, right coronary arteriographies revealed severely delayed filling of contrast medium without significant narrowing of epicardial coronary arteries, suggesting microembolism or microvascular vasospasm. An intracoronary infusion of isosorbide dinitrate did not improve the delayed filling of contrast medium or ST segment depression on ECG. Soon after intracoronary infusion of diltiazem in case 1 and nicorandil in case 2, coronary arterial flows were normalized, chest symptoms disappeared, and ECG findings were normalized. The next day, both patients' 99mTc-tetrofosmin myocardial SPECT showed normal uptake. These findings suggest that myocardial ischemia in these cases might be explained as having been caused by microvascular spasm.

Calcium Channel Blockers↗
PubMed2006

Transcardiac adiponectin gradient is independently related to endothelial vasomotor function in large and resistance coronary arteries in humans.

Adiponectin, an adipocyte-derived protein, has been shown to have vasculoprotective effects. This study examined the possible relationship between coronary vasomotor function and the transcardiac gradient of adiponectin, reflecting adiponectin utilization and/or accumulation in the coronary vascular bed. The epicardial diameter and blood flow response of the left anterior descending coronary artery to intracoronary infusions of ACh was analyzed in 108 consecutive subjects who had a normal coronary angiogram and left ventriculogram. Adiponectin levels were measured by ELISA in plasma obtained from the aortic root (Ao) and the anterior interventricular vein (AIV). Adiponectin levels in the AIV were lower than levels in the Ao. In multivariate linear regression analysis, the transcardiac gradient of adiponectin (Ao - AIV levels) showed a positive correlation with increases in epicardial coronary diameter and coronary blood flow in response to ACh that was independent of traditional coronary risk factors. The transcardiac gradient of adiponectin was not significantly associated with the coronary dilator response to isosorbide dinitrate and the coronary flow response to sodium nitroprusside. In other groups of patients with coronary spastic angina (n = 41) or microvascular angina (n = 32) who had impaired coronary vasomotor responses, there was no significant gradient of adiponectin between the Ao and AIV. The transcardiac gradient of adiponectin may modulate endothelial vasomotor function in large and resistance coronary arteries and may play a role in the pathogenesis of diseases presenting with coronary vasomotor dysfunction.

Adiponectin↗
PubMed1997

Impact of impaired coronary flow reserve and insulin resistance on myocardial energy metabolism in patients with syndrome X.

To evaluate the role of a decreased coronary flow reserve in the genesis of angina pectoris in patients with syndrome X, we studied myocardial hemodynamics and metabolism at rest, during pace stress, and in the recovery period after pacing in 18 consecutive patients with syndrome X and in 10 control subjects. By means of positron emission tomography or the intracoronary flow-wire method, patients were subclassified as having microvascular angina (MA, n = 8) when coronary flow reserve was reduced (<2.5) or no microvascular angina (non-MA, n = 10) when coronary flow reserve was preserved (> or =2.5). At rest, coronary sinus blood flow was increased in MA patients. During pace stress, coronary sinus blood flow increased by 39 +/- 6% in MA patients versus 67 +/- 12% in non-MA patients and 69 +/- 7% in controls (p <0.05). Patients with non-MA revealed fasting hyperinsulinemia, increased arterial concentration of free fatty acids, and a similar tendency for beta-hydroxybutyrate. Oxygen extraction and carbon dioxide release did not differ between groups. Net myocardial lactate release was not observed in any patient during pace stress and myocardial energy metabolism was preserved in all patients with syndrome X. During pacing, myocardial uptake of free fatty acids and beta-hydroxybutyrate was increased in non-MA patients. Myocardial uptake of free fatty acids correlated positively and myocardial glucose and lactate uptake correlated inversely with arterial concentrations of free fatty acids in all subjects. Metabolic evidence of myocardial ischemia is uncommon in patients with syndrome X, irrespective of a globally reduced coronary flow reserve. Although patients with syndrome X can be subclassified according to presence of a microvascular or a metabolic disorder, angina pectoris and ST-segment depressions coexist with a preserved global myocardial energy efficiency in all patients.

Cardiac Pacing, Artificial↗
PubMed2002

Reduced microvascular and myocardial damage in patients with acute myocardial infarction and preinfarction angina.

BACKGROUND: After acute myocardial infarction, the presence of ischemic preconditioning as a result of preinfarction angina has a protective role, limiting necrosis extent and guaranteeing greater myocardial functional recovery. The relationship between preinfarction angina, microvascular reflow, and myocardial function is poorly known. We hypothesized that after acute myocardial infarction patients with preinfarction angina have both microvascular integrity and myocardial function preservation. METHODS AND RESULTS: In 51 patients with a first acute myocardial infarction, we noninvasively assessed microvascular perfusion and coronary flow reserve with intravenous myocardial contrast echocardiography and investigated myocardial contractile recovery with low-dose dobutamine and 90-day follow-up echocardiography. Typical angina was present in 25 patients and absent in 26 patients during the 7 days preceding the myocardial infarction. Compared with those patients without preinfarction angina, patients with preinfarction angina showed a greater microvascular reflow extent and coronary flow reserve (respectively, 25.2% +/- 22.8% vs 48.3% +/- 23.3%, P <.05, and 3.44 +/- 0.75 vs 1.95 +/- 0.67, P <.0001), a better regional myocardial function, as expressed with wall motion score index in the risk area at dobutamine (1.67 +/- 0.61 vs 2.10 +/- 0.43, P <.005) and at follow-up (1.72 +/- 0.56 vs 2.22 +/- 0.40, P <.0001) echocardiogram, despite being similar in the first echocardiogram (2.60 +/- 0.28 vs 2.63 +/- 0.28, P = not significant), and significantly less pronounced left ventricular dilation at follow-up. CONCLUSION: Presence of preinfarction angina, because of the preconditioning effect, reduces myocardial damage and favors myocardial viability, limiting left ventricular remodeling. This beneficial effect seems to be at least partly mediated by the more preserved microvascular integrity and functional vasodilation after acute myocardial infarction.

Angina, Unstable↗
PubMed1996

Cardiovascular syndromes X, endothelial dysfunction and insulin resistance.

Cardiac Syndrome X (microvascular angina) and the more recently described metabolic Syndrome X (an epidemiological association between insulin resistance and atheroma, dyslipidaemia, and hypertension) may have more in common than the chance of their common sobriquet, in view of evidence that microvascular angina too is characterised by insulin resistance and endothelial dysfunction. The implications are discussed.

Endothelium, Vascular↗
PubMed1992

[The dilemma of syndrome X].

The term X syndrome involves several dilemmas. The terminological dilemma is that this term is used to describe microvascular angina pectoris, as well as Reaven's metabolic-hormonal syndrome and our 5H syndrome [association of hyperinsulinism with arterial hypertension, hyperlipoproteinaemia, hyperglycaemia (NIDDM) and hirsutism]. It is probable that the coronary X syndrome is frequently conditioned by the hormonal-metabolic X syndrome. The pathogenetic dilemma is that it is not clear why in microvascular angina pectoris the coronary circulation does not possess an adequate reserve for vasodilatation during exercise or in response to some pharmacological stimuli. This could condition hyperinsulinism in hypertonic subjects with NIDDM with an early disorder of paracrine endothelial relaxation mechanisms (EDRF-NO), with a predominance of vasoconstrictor mechanisms (endothelin-1). In Reaven's syndrome X it is not clear whether insulin resistance of the postreceptor type is a primary inborn phenomenon which is compensated by insulin hypersecretion or whether it is a secondary phenomenon, which develops ex post and by which the target tissues defend themselves against an excessive effect of insulin (e.g. down regulation receptors) in primary disorders of its secretion.

Angina Pectoris↗
PubMed1989

Panic disorder in patients with chest pain and angiographically normal coronary arteries.

Although patients with angiographically normal or near normal coronary arteries are at low risk for cardiac disease, several follow-up studies have shown that many continue to report recurrent chest pain associated with social and work dysfunction. Three diagnostic entities have been proposed to explain the morbidity of this group: microvascular angina, esophageal motility disorders and panic disorder. The purpose of this study was to test the hypothesis that panic disorder is found frequently in patients with chest pain who have normal epicardial vessels. Ninety-four subjects with angiographically normal coronary arteries were interviewed according to a structured psychiatric protocol within 24 hours of their catheterizations. Thirty-two (34%) fit Diagnostic and Statistical Manual of Mental Disorders (third edition, revised) criteria for current panic disorder. Because panic disorder can be effectively treated, physicians should consider this diagnosis in this group of patients. Current research findings suggest that panic disorder, microvascular angina and esophageal disorders may each form the basis for chest pain in approximately 25% of these patients. Miscellaneous problems account for the other 25%.

Adult↗
PubMed1996

Angina with normal coronary arteries: diagnosis, pathophysiology and treatment.

Approximately 20% of patients undergoing diagnostic coronary arteriography for acute or chronic cardiac ischaemia have angiographically normal coronary arteries. The mechanism behind this phenomenon is likely to be the result of a combination of functional or anatomical abnormalities in the coronary microcirculation, a metabolic disorder which affects the handling of energy substrates by the heart, insulin resistance and a neurological component affecting pain perception. Indeed, it has been demonstrated that these patients often exhibit an increase in sympathetic outflow to the cardiovascular system, which might account for the reduction in coronary flow reserve, changes in metabolic utilization and development of insulin resistance that are seen in some of these patients. Therapeutically, beta-blockers appear to be most effective in controlling the symptoms associated with this condition, although those calcium antagonists which do not affect the neurohormonal system may be of some utility in patients with primary microvascular angina, in which microvascular spasm is operating or in whom excessive constriction of the distal component of the coronary circulation limits the vasodilatory reserve.

Adrenergic beta-Antagonists↗
PubMed1998

Enhanced insulin response to oral glucose load in patients with angina pectoris associated with ST segment elevation in the absence of epicardial coronary arterial obstruction.

The authors treated 10 patients with microvascular angina (MVA) manifesting angina pectoris, ST segment elevation suggestive of transmural myocardial ischemia, and no epicardial arterial obstruction. Since such patients frequently showed abnormal responses to oral glucose loading, the authors investigated the glucose and insulin responses to glucose loading in 10 MVA patients, 25 patients with vasospastic angina (VAP), 25 patients with effort angina (EAP), and 25 control subjects. Insulinogenic index, peripheral insulin activity [= 10(4)/(peak glucose x insulin at glucose peak)], glucose area, and insulin area were calculated. The MVA group included two patients with impaired glucose tolerance and two newly diagnosed diabetic patients. These proportions were similar to those in the VAP and EAP groups. Glucose levels at 30 to 180 min and insulin levels at 90 to 120 min in the MVA group were higher than in the control group. Peak glucose, glucose area, peak insulin, and insulin area were higher in the MVA group than in the control group (p<0.01). Those in the VAP and EAP groups were also higher. Insulin/glucose ratio at 120 min was higher, peripheral insulin activity, lower, in the disease groups than in the control group (p<0.05). The MVA patients showed a hyperglycemic and hyperinsulinemic response to oral glucose loading, as did the patients with EAP and VAP. Enhanced insulin response to oral glucose loading may also contribute to the pathogenesis of MVA.

Adult↗
PubMed1998

Plasma endothelin-1 levels in patients with angina pectoris and normal coronary angiograms.

BACKGROUND: Some patients with typical angina and electrocardiographic evidence of ischemia have normal coronary angiograms. These patients have a reduced coronary flow reserve and abnormal endothelium-dependent vasodilator responses; this syndrome is known as microvascular angina. Among endothelium-derived peptides, endothelin-1 (ET-1) is a potent vasoconstrictor and an important modulator of microvascular function. METHODS: Plasma ET-1 was measured in 13 patients with typical angina, instrumental evidence of ischemia, and normal arteriograms and in 20 normal control subjects. RESULTS: Mean concentration of ET-1 was 2.89+/-1.24 pmol/L in patients with angina and normal angiograms and 1.99+/-0.81 pmol/L in normal control subjects (p < 0.02). Plasma levels of ET-1 values were significantly higher in patients with angina, positive exercise test results for ischemia, and normal coronary arteriograms compared with the group of patients with no clinical or instrumental evidence of ischemia. CONCLUSIONS: This is consistent with the hypothesis that in patients with microvascular angina, an endothelial dysfunction in the coronary vascular area caused by impaired endothelium-derived ET-1 could play an active role in the disease process.

Adult↗
PubMed1995

Autonomic balance in patients with angina and a normal coronary angiogram.

The pathophysiology of angina pectoris in patients with a normal coronary angiogram is not clear. Furthermore, the pathophysiological impact of ST changes in syndrome X is controversial. The purpose of this study was to investigate cardiac autonomic function, by measuring 24 h heart rate variability, in patients with and without electrocardiographic evidence of ischaemia during exercise. Thirty-two patients with angina pectoris, a normal coronary angiogram, echocardiogram, hyperventilation test and gastro-oesophageal investigation were studied. Fourteen healthy subjects served as controls. Fifteen patients had significant ST segment depression during stress testing, whereas 17 had no electrocardiographic signs of ischaemia. Heart rate variability was calculated as (1) mean RR = mean of all normal RR intervals, (2) the difference in mean RR level between when awake and when asleep (mean RR wake-sleep)-a tentative index of sympathetic activation, (3) the standard deviation (SD)-a broad band measure of autonomic balance, and (4) a percentage of successive RR interval differences > or = 6% (pNN6%)-an index of vagal modulation. The coronary vascular resistance was measured at rest and during pacing. Mean RR and autonomic indexes did not differ between patients with a positive exercise test and controls (831/884 ms; 24 h SD 125/134 ms; pNN6% 6.715.4%, respectively). Patients with a normal exercise test had shorter mean RR (758 ms vs 844 ms; P < 0.05) and significantly reduced 24-h SD (103 ms vs 134 ms; P < 0.05) than controls, whereas values for vagal index (6.5% vs 5.4%) did not differ from healthy controls. Mean RR wake-sleep also tended to be lower in patients with a normal exercise test (-125 ms vs -173 ms) compared to controls (P < 0.1). Patients with a positive exercise test had a significantly attenuated reduction in coronary vascular resistance during pacing in comparison to patients with a normal exercise test (-0.131 -0.26 mmHg x min. ml-1; P < 0.05). The findings suggest the occurrence of general elevated sympathetic activation in angina patients with a normal exercise test. Patients with a positive exercise test exhibited no signs of autonomic dysfunction although these patients had altered coronary vascular resistance indicating microvascular angina. This supports the suggestion that patients with a normal exercise test constitute an independent pathophysiological entity.

Adult↗
PubMed1995

Angina pectoris and normal coronary arteriograms: clinical presentation and hemodynamic characteristics.

Up to 30% of patients undergoing coronary angiography for the assessment of chest pain suggestive of coronary artery disease have "normal" studies. Several reports have indicated that a proportion of patients with angina and normal coronary arteriograms have reduced coronary flow reserve. The interpretation of these findings is, however, controversial as the majority of patients do not have definitive evidence for myocardial ischemia and have a good long-term prognosis. The clinical presentation of patients with angina and normal coronary arteriograms differs in different series and this may be just a reflection of the heterogeneous nature of the syndrome. A diversity of pathogenetic mechanisms have been postulated to explain "syndrome X" (chest pain and normal coronary arteriograms) but little is known at present about the true nature of the syndrome. The present article discusses the clinical and hemodynamic features of this intriguing disorder with particular reference to patients with syndrome X and microvascular angina.

Angina Pectoris↗
PubMed1989

Gastro-oesophageal reflux disease, an important cause of angina-like chest pain.

Angina-like chest pain in patients with coronary arteriography raises difficult diagnostic problems. The pain may be due to microvascular angina (or syndrome X). It is postulated that during the typical angina of these patients, the ST segment shifts on exercise electrocardiogram and the abnormal electrophysiologic tests on cardiac catheterisation are due to a decreased coronary flow reserve related to microvascular abnormalities. Angina-like chest pain may also be of oesophageal origin. Gastro-oesophageal reflux and oesophageal motility disorders are the two commonest oesophageal abnormalities held responsible for the pain. Recent observations suggest that sensitivity of the oesophagus to several stimuli may be another important cause of chest pain of oesophageal origin. This condition is called irritable oesophagus. Twenty-four hour pH- and pressure-recording is at present the best way to reach a specific diagnosis about the nature of the oesophageal abnormality.

Angina Pectoris↗
PubMed1992

Thallium scans in syndrome X.

OBJECTIVE: To review thallium scans in patients with angina and normal coronary arteriograms. DESIGN: Retrospective review of data. SETTING: Regional cardiac centre in Glasgow. PATIENTS: 100 patients selected from those undergoing diagnostic angiography for typical angina who had normal arteriograms (around 10%), no other cardiovascular abnormality, and available thallium scans (performed routinely before angiography). MAIN OUTCOME MEASURES: Coronary arteriography, exercise tests, and gated thallium scans at peak exercise. RESULTS: The exercise test was positive in 30 and negative in 70 patients. Thallium defects were found in 98 patients, but no consistent pattern and no significant correlation existed between the extent of thallium defect and positive exercise test or exercise tolerance. CONCLUSIONS: Thallium defects described in 98 of 100 patients with angina and normal coronary arteriograms suggest that microvascular angina may be commoner than is generally appreciated.

Adult↗