Dental fear with and without blood-injection fear: implications for dental health and clinical practice

BACKGROUND: It has been suggested that the sympathetic nervous system might play an important role in the development of coronary artery spasm. However, no cardiac imaging modality has been able to demonstrate abnormal sympathetic innervation in patients with coronary artery spasm. The purpose of this study was to assess the presence and location of abnormal sympathetic innervation using iodine 123-metaiodobenzylguanidine (123I-MIBG) single photon emission computed tomography (SPECT) and to evaluate the clinical efficacy of 123I-MIBG SPECT as a noninvasive screening test in patients with coronary artery spasm. METHODS AND RESULTS: Coronary arteriography and a provocative test with intravenous administration of ergonovine maleate were performed in 26 patients (20 men, 6 women, mean age 48.2+/-12.0 years, range 20 to 67 years) who were suspected of having a coronary artery spasm. The subjects were divided into 2 groups: group 1 (n = 18) comprised subjects with a positive provocative test result, and group 2 (n = 8) comprised subjects with negative provocative test results. Ten healthy subjects served as controls. No abnormal MIBG uptake was observed in the control subjects. Abnormal sympathetic nervous innervation using 123I-MIBG SPECT was observed either as a reduced uptake or a defective pattern in the perfused areas in 13 of the 18 regions supplied by vessels of ergonovine-induced vasospasm. Normal sympathetic innervation, as evidenced by normal 123I-MIBG uptake, was noted in all of the 60 segments of normal vessel territories. Reduced uptake of 123I-MIBG was not detected in the perfused areas of 5 vasospasm-induced vessels (perfusion territory of left anterior descending coronary artery [LAD] and the right coronary artery [RCA] in 2 and 3 patients, respectively). The sensitivity and specificity of 123I-MIBG for detection of coronary artery spasm were 72.2% (95% confidence interval [CI] 55% to 89%) and 100%, respectively. The positive predictive and negative predictive values were 100% and 92.3% (95% CI 91% to 93%), respectively. CONCLUSION: 123I-MIBG SPECT is a feasible method to evaluate noninvasively and localize the territories of coronary arteries with spasm. Invasive diagnostic coronary arteriography with ergonovine provocation test may be unnecessary for diagnosis of coronary artery spasm in patients with typical resting pain, negative exercise test or normal thallium perfusion scan results, but showing abnormalities in 123I-MIBG SPECT.     

Spontaneously and pharmacologically provoked coronary arterial spasm in Prinzmetal variant angina

Eleven of 21 consecutive patients with Prinzmetal angina (PMA) exhibited no significant fixed stenoses of the coronary arteries. Spontaneous coronary arterial spasm was demonstrated in 3 patients. Ergonovine maleate produced near-total occlusion of a major vessel in 3 of 4 other patients with PMA, but did not provoke spasm in 10 without PMA. The current study documents spasm as the mechanism of myocardial ischemia in some patients with normal coronary arteries and provides initial and favorable diagnostic results with provocative pharmacoangiography in this entity.     

Acute myocardial infarction during pregnancy caused by coronary artery spasm

A 33-year-old pregnant woman suffered from acute anteroseptal myocardial infarction at the 19th gestational week. Despite periodic attacks of myocardial ischaemia after admission, the coronary arteriograms under the use of nitroglycerin were normal. Thereafter, she remained free from the ischaemic events with diltiazem hydrochloride and delivered a healthy baby. The coronary arteriography at puerperium also showed no organic narrowing. However, the provocative test with acetylcholine chloride caused severe spasm of the left anterior descending coronary artery. These findings strongly suggest that acute myocardial infarction in this pregnant woman was caused by coronary artery spasm.     

Myocardial infarct with a normal coronary angiogram

The present report describes a case of a massive transmural anterior wall myocardial infarction in a woman with angiographically normal coronary arteries. The possible mechanisms of production of myocardial infarction in the presence of normal coronary arteriograms are discussed. With the increasing application of coronary arteriography, such diagnostic problems will undoubtedly become more frequent.     

Angina pectoris caused by coronary microvascular spasm

BACKGROUND: Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest. METHODS: Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (>50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein. FINDINGS: Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p<0.01) and fewer coronary risk factors (p<0.01) in patients with microvascular spasm than in those with large-artery spasm. INTERPRETATION: Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.     

Sublabial, transseptal, transsphenoidal approach to the pituitary region guided by the ACUSTAR I system

Myocardial infarction occurring in young people with angiographically normal coronary arteries is well described but the pathophysiology of this condition remains unknown. Coronary artery spasm in association with thrombus formation and minimal atheromatous disease or spontaneous coronary artery dissection are possible causes. Two young men presented with severe chest pain after acute alcohol intoxication and each sustained an extensive anterior myocardial infarction. Investigations including intravascular ultrasound showed no evidence of atherosclerotic coronary artery disease. Coronary artery spasm associated with acute alcohol intoxication as well as prothrombotic state and endothelial damage related to cigarette smoking may be mechanisms leading to acute myocardial infarction in these cases. Acute myocardial infarction occurs in young persons with normal coronary arteries and the diagnosis should be considered in young patients presenting with severe chest pain, particularly those abusing cocaine or alcohol, so that reperfusion therapy can be initiated promptly.     

Selective correlation of amide groups to glycine alpha protons and of arginine guanidine groups to delta protons in proteins by multiple quantum spectroscopy

Study objective: We sought to determine whether electron-beam computed tomography (EBCT) could be used as a triage tool in the emergency department for patients with angina-like chest pain, no known history of coronary disease, normal or indeterminate ECG findings, and normal initial cardiac enzyme concentrations. METHODS: We conducted a prospective observational study of 105 patients admitted between December 1995 and October 1997 to the ED of a large tertiary care hospital with 70,000 annual ED visits. The study group was comprised of women aged 40 to 65 years and men aged 30 to 55 years who presented with angina-like chest pain requiring admission to the hospital or chest pain observation unit. All patients underwent EBCT of the coronary arteries, along with other cardiac testing as deemed necessary by staff physicians. RESULTS: Of the 105 patients, 100 underwent other cardiac testing during hospitalization. Evaluation included treadmill exercise testing in 58, coronary angiography in 25, radionuclide stress testing in 19, and echocardiography in 11. Results of EBCT and cardiac testing were negative for both in 53 patients (53%), positive for both in 14 (14%), positive for tomography and negative for cardiac testing in 32 (32%), and negative for tomography and positive for cardiac testing in only 1 patient. This positive test result, on a treadmill exercise test, was ruled a false positive by an independent staff cardiologist. Two other female patients with normal exercise sestamibi or coronary angiography and EBCT findings also had false-positive treadmill exercise results. The sensitivity of EBCT was 100% (95% confidence interval, 77% to 100%), with a negative predictive value of 100% (95% confidence interval, 94% to 100%). Specificity was 63% (95% confidence interval, 54% to 75%). CONCLUSION: EBCT is a rapid and efficient screening tool for patients admitted to the ED with angina-like chest pain, normal cardiac enzyme concentrations, indeterminate ECG findings, and no history of coronary artery disease. Our study suggests that patients with normal initial cardiac enzyme concentrations, normal or indeterminate ECG findings, and negative results on EBCT may be safely discharged from the ED without further testing or observation. Larger studies are required to confirm this conclusion.     

Association between myocardial infarction and the mast cells in the adventitia of the infarct-related coronary artery

BACKGROUND: Histamine, a product of mast cells, is an effective vasoconstrictor of atherosclerotic coronary arteries. Because it has been suggested that coronary spasm plays a role in acute coronary syndromes such as myocardial infarction (MI), we quantified and characterized the mast cells in the adventitia of infarct-related coronary arteries. METHODS AND RESULTS: In a series of 17 autopsied MI patients, we identified the segment of the left coronary artery with ruptured plaque responsible for the infarction. More distal segments from the infarct-related coronary artery, either with nonruptured plaques or with normal intima, were also studied. Corresponding segments taken from left coronary arteries obtained from 17 patients who had died of noncardiac causes served as controls. Adventitial mast cells in the infarct-related and the control coronary arteries were identified immunohistochemically by staining for tryptase. In the infarct-related coronary arteries, we also stained for chymase and histamine. Moreover, T lymphocytes and macrophages were identified immunohistochemically and counted. In the infarct-related coronary arteries, significantly larger numbers of mast cells were present in the adventitia backing ruptured plaques (98+/-40 mast cells/mm2, mean+/-SD) than in the adventitia backing nonruptured plaques (41+/-12 mast cells/mm2; P<0.001) or backing normal intima (19+/-8 mast cells/mm2; P<0.001). No such difference was found among the 3 different segments in the control coronary arteries. The majority of mast cells contained not only tryptase but also chymase. Mast cells were the only cells in the coronary adventitia that contained histamine. The proportion of adventitial mast cells that were degranulated was highest in the segments with ruptured plaques. The numbers of adventitial macrophages and T lymphocytes were also increased in the segments with plaque rupture. CONCLUSIONS: In infarct-related coronary arteries, the number of degranulated mast cells in the adventitia backing ruptured plaques is increased. Histamine released from the degranulated mast cells may reach the media, where it may locally provoke coronary spasm and thus contribute to the onset of MI.     

Selective ergonovine-induced coronary artery spasm and ST-segment alternans after blunt thoracic trauma

A 24-year-old man was found to have angiographically normal coronary arteries shortly after suffering blunt thoracic trauma. Selective ergonovine administration into the left coronary artery induced total occlusion of the left anterior descending branch and electrical alternans of the ST-segment. This case demonstrates coronary artery spasm as a possible mechanism of coronary occlusion after blunt thoracic trauma.     

Detection of severity of coronary stenosis by quantitative myocardial tomography with Tc-99m-MIBI at rest

To evaluate the role of myocardial tomography with Tc-99m-MIBI (MB) in detecting abnormal coronary arteries, 34 patients with myocardial infarction underwent resting quantitative SPEC with MB and coronary arteriography within one month. When segmental MB uptake was < 560% of the left ventricular peak activity, there was 88% probability that a totally occluded or severely stenosed coronary artery (stenosis > 90%) was involved. There was 82% probability of finding no significant stenosis of coronary arteries in the normal myocardial segments. In the myocardial segments supplied by occluded coronary arteries, there was significantly higher MB uptake in the segments with good collateral circulation as compared with those subtended by a vessel totally occluded with poor collateral circulation (P < 0.05). The sensitivity and specificity of detecting abnormal coronary artery by quantitative analysis of myocardial tomography was 87% and 90% respectively. It is suggested that quantitative analysis of myocardial tomography with MB can differentiate between myocardial segments supplied by severely stenosed and normal coronary artery and evaluate the existence of collateral circulation.     

Acute myocardial infarction related to cocaine use. Report of a case

Cocaine use has been associated with ischemic syndromes, especially angor pectoris, myocardial infarction, cardiac arrhythmias and sudden death. A significant number of persons suffering from myocardial infarction associated with cocaine abuse do not have significant coronary atherosclerosis, and the mechanism for infarction in these patients have remained obscure. This report describes a young man with angiographically normal coronary arteries in whom cocaine abuse probably produced coronary artery spasm leading to coronary thrombosis and infarction.     

A new noninvasive method of diagnosing vasospastic angina based on dilation response of the left main coronary artery to nitroglycerin as measured by echocardiography

OBJECTIVES: The purpose of the present study was to evaluate the feasibility of diagnosing vasospastic angina based on coronary artery tone as assessed by M-mode echocardiographic measurement of the dilation response of the left main coronary artery to nitroglycerin. BACKGROUND: The definite diagnosis of vasospastic angina is done by a coronary spasm provocative test using ergonovine maleate or acetylcholine during cardiac catheterization. Current noninvasive, nonpharmacologic diagnostic methods are not sensitive enough for the diagnosis of vasospastic angina. METHODS: Thirty-eight patients who had an angiographically normal left main trunk were studied. These patients were classified into four groups based on the presence or absence of more than 50% stenosis in the coronary arteries except for the left main trunk and the results of the acetylcholine or ergonovine provocative test. At 7 a.m. and at noon on the same day, the left main trunk diameter was measured by M-mode echocardiography before and after sublingual administration of nitroglycerin (0.3 mg), and its present dilation was calculated to assess coronary artery tone. RESULTS: The percent dilation of the left main trunk diameter induced by sublingual nitroglycerin at 7 a.m. and at noon was 22.4 +/- 4.7% (mean +/- SD) and 18.1 +/- 4.0% in 11 patients with vasospastic angina and without coronary stenosis, 14.9 +/- 7.1% and 11.2 +/- 6.9% in 9 patients with vasospastic angina and coronary stenosis, 6.1 +/- 3.5% and 7.0 +/- 5.1% in 8 patients without vasospastic angina but with coronary stenosis and 8.1 +/- 5.6% and 7.8 +/- 5.7% in 10 control subjects. The percent dilation at 7 a.m. was significantly greater in the vasospastic angina without coronary stenosis group than in the remaining three groups, and in the vasospastic angina groups, the percent dilation at 7 a.m. was significantly greater than that at noon. When percent dilation at 7 a.m. exceeding 15% was defined as positive for the diagnosis of vasospastic angina, the sensitivity was 80% and the specificity 94%. CONCLUSIONS: Basal tone of the left main trunk is elevated in the early morning in vasospastic angina. Dilation of the left main trunk diameter exceeding 15% induced by sublingual nitroglycerin in the early morning as measured by M-mode echocardiography is a highly sensitive and specific criterion for the diagnosis of vasospastic angina.     

Soluble P-selectin is released into the coronary circulation after coronary spasm

BACKGROUND: The glycoprotein P-selectin is an adhesion molecule involved in the property change of leukocytes at the initiation of the inflammatory process. The purpose of the present study was to determine whether acute myocardial ischemia induced by coronary spasm causes an acute inflammatory response in the coronary circulation. METHODS AND RESULTS: We examined plasma soluble P-selectin levels in the coronary sinus and the aortic root simultaneously in 16 patients with coronary spastic angina before and after left coronary artery spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Ten control patients with chest pain but normal coronary arteries and no coronary spasm also received intracoronary acetylcholine. Plasma soluble P-selectin levels were increased significantly in the coronary sinus (32.8 +/- 3.6 to 52.8 +/- 5.9 ng/mL, P < .001) and in the aortic root (34.6 +/- 3.7 to 41.9 +/- 4.4 ng/mL, P < .05) after the attacks in the coronary spastic angina group but remained unchanged in the stable exertional angina group after the attacks and in the control group after the administration of acetylcholine. Furthermore, the coronary sinus-arterial difference of soluble P-selectin increased significantly after the attacks in the coronary spastic angina group (-1.8 +/- 2.2 to 10.9 +/- 2.7 ng/mL, P < .001). CONCLUSIONS: Our data indicate that soluble P-selectin is released into the coronary circulation after coronary artery spasm. We conclude that coronary artery spasm may induce the leukocyte adhesion in the coronary circulation and may lead to myocardial damage.     

Improved detection of coronary artery disease by exercise electrocardiography with the use of right precordial leads

BACKGROUND: Exercise electrocardiography is an perfect test for the detection of coronary artery disease. We attempted to improve the diagnostic accuracy of exercise testing as a noninvasive method for the detection of coronary artery disease by using a combination of the left and right precordial leads. METHODS: We studied 245 patients (218 men and 27 women) ranging from 32 to 74 years of age (mean [+/-SD], 52+/-8) who underwent treadmill exercise testing, thallium-201 scintigraphy, and coronary arteriography. During exercise testing, each patient had one electrocardiogram recorded with the standard 12 leads and 3 right precordial leads (V3R, V4R, and V5R), with the results for each set of leads recorded and analyzed separately. RESULTS: On the basis of coronary arteriography, 34 patients had normal coronary arteries, 85 had single-vessel disease, 84 had two-vessel disease, and 42 had three-vessel disease. The sensitivities of the standard 12-lead exercise electrocardiogram, exercise electrocardiography incorporating right precordial leads, and thallium-201 scintigraphy were 52 percent, 89 percent, and 87 percent, respectively, for the detection of single-vessel disease; 71 percent, 94 percent, and 96 percent for the detection of two-vessel disease; 83 percent, 95 percent, and 98 percent for the detection of three-vessel disease; and 66 percent, 92 percent, and 93 percent for the detection of any coronary artery disease. The specificities of the three methods for the detection of any coronary artery disease were 88 percent, 88 percent, and 82 percent, respectively. CONCLUSIONS: Use of right precordial leads along with the standard six left precordial leads during exercise electrocardiography greatly improves the sensitivity of exercise testing for the diagnosis of coronary artery disease.     

Percutaneous transluminal coronary angioplasty reverses vasoconstriction of stenotic coronary arteries in hypertensive patients

BACKGROUND: Endothelial dysfunction of coronary arteries with impaired vasodilation has been reported in patients with arterial hypertension. However, the effect of dynamic exercise on coronary vasomotion of a stenotic vessel segment before and after PTCA has not yet been evaluated in these patients. METHODS AND RESULTS:Coronary vasomotion of a normal and a stenotic vessel segment was studied in 39 patients with coronary artery disease during supine bicycle exercise before and 9+/-3 months after PTCA. Luminal area changes were determined by biplane quantitative coronary arteriography. There were 21 normotensive and 18 hypertensive patients who did not differ with regard to clinical characteristics. Percent area stenosis decreased after PTCA from 90% to 39% (P<0.001) in normotensive and from 86% to 33% (P<0.001) in hypertensive patients. Exercise-induced vasomotion of the normal vessel segment was significantly different between normotensives and hypertensives before (+19% versus +1%, P<0.01) and after (+16% versus +3%, P<0.01) PTCA. In contrast, stenotic vessel segments showed vasoconstriction in both normotensive and hypertensive patients (Deltaexercise, -11% versus - 20%, P=NS), which was reversed after PTCA (+3% versus +2%, P=NS). CONCLUSIONS: Normal coronary arteries show reduced vasodilation during exercise in hypertensive patients that may be explained by the presence of endothelial dysfunction. Stenotic vessels demonstrate paradoxical vasoconstriction during exercise in both normotensive and hypertensive patients. PTCA reverses vasoconstriction by elimination of the flow-limiting stenosis and prevention of coronary stenosis narrowing during exercise in normotensive and hypertensive patients.     

Enhanced myosin light chain phosphorylations as a central mechanism for coronary artery spasm in a swine model with interleukin-1beta

BACKGROUND: Although coronary artery spasm plays an important role in a wide variety of ischemic heart diseases, the intracellular mechanism for the spasm remains to be clarified. We examined the role of myosin light chain (MLC) phosphorylations, a key mechanism for contraction of vascular smooth muscle, in our swine model with interleukin-1beta (IL-1beta). METHODS AND RESULTS: IL-1beta was applied chronically to the porcine coronary arteries from the adventitia to induce an inflammatory/proliferative lesion. Two weeks after the operation, intracoronary serotonin repeatedly induced coronary hyperconstrictions at the IL-1beta-treated site both in vivo and in vitro, which were markedly inhibited by fasudil, an inhibitor of protein kinases, including protein kinase C and MLC kinase. Western blot analysis showed that during serotonin-induced contractions, MLC monophosphorylation was significantly increased and sustained in the spastic segment compared with the control segment, whereas MLC diphosphorylation was noted only in the spastic segment. A significant correlation was noted between the serotonin-induced contractions and MLC phosphorylations. Both types of MLC phosphorylation were markedly inhibited by fasudil. In addition, MLC diphosphorylation was never induced by a simple endothelium removal in the normal coronary artery, whereas enhanced MLC phosphorylations in the spastic segment were noted regardless of the presence or absence of the endothelium. CONCLUSIONS: These results indicate that enhanced MLC phosphorylations in the vascular smooth muscle play a central role in the pathogenesis of coronary spasm in our swine model.     

Variations in normal coronary vasodilatory reserve stratified by artery, gender, heart transplantation and coronary artery disease

OBJECTIVES: The purpose of the study was to assess the spectrum of coronary vasodilatory reserve values in patients with angiographically normal arteries who had atypical chest pain syndromes or remote coronary artery disease or were heart transplant recipients. BACKGROUND: The measurement of post-stenotic coronary vasodilatory reserve, now possible in a large number of patients in the cardiac catheterization laboratory, is increasingly used for decision making. Controversy exists regarding the range of normal values obtained in angiographically normal coronary arteries in patients with different clinical presentations. METHODS: Quantitative coronary arteriography was performed in 214 patients classified into three groups: 85 patients with chest pain syndromes and angiographically normal arteries (group 1); 21 patients with one normal vessel and at least one vessel with > 50% diameter lumen narrowing (group 2); and 108 heart transplant recipients (group 3). Coronary vasodilatory reserve (the ratio of maximal to basal average coronary flow velocity) was measured in 416 arteries using a 0.018-in. (0.04 cm) Doppler-tipped angioplasty guide wire. Intracoronary adenosine (8 to 18 micrograms) was used to produce maximal hyperemia. RESULTS: Coronary vasodilatory reserve was higher in angiographically normal arteries in patients with chest pain syndromes (group 1:2.80 +/- 0.6 [group mean +/- SD]) than in normal vessels in patients with remote coronary artery disease (group 2: 2.5 +/- 0.95, p = 0.04); both values were significantly higher than those in the post-stenotic segment of the diseased artery (1.8 +/- 0.6, p < 0.007). Coronary vasodilatory reserve in transplant recipients (group 3) was higher than that in the other groups (3.1 +/- 0.9, p < 0.05 vs. groups 1 and 2) as a group and for individual arteries. When stratified by vessel, coronary vasodilatory reserve was similar among the left anterior descending, left circumflex and right coronary arteries. There were no differences between coronary vasodilatory reserve values on the basis of gender for patients with coronary artery disease and transplant recipients. In group 1 (chest pain), there was a trend toward higher coronary vasodilatory reserve in men than in women (2.9 +/- 0.6 vs 2.7 +/- 0.6, p = 0.07). CONCLUSIONS: These findings identify a normal reference range for studies assessing the coronary circulation and post-stenotic coronary vasodilatory reserve in patients with and without coronary artery disease encountered in the cardiac catheterization laboratory.     

Improved specificity of transesophageal dobutamine stress echocardiography compared to standard tests for evaluation of coronary artery disease in women presenting with chest pain

The detection of coronary artery disease (CAD) by noninvasive methods has been hindered in women by the high rate of false-positive results. To determine the feasibility and accuracy of transesophageal dobutamine stress echocardiography for identification of CAD in women, we studied 84 patients (age 51 +/- 11 years) who underwent symptom-limited exercise treadmill testing, exercise thallium-201 scintigraphy, and coronary angiography for evaluation of anginal chest pain. Of the 84 patients, 62 had normal coronary arteries or nonsignificant coronary lesions, and 22 had significant stenosis of > or = 1 major coronary artery. During treadmill exercise, repolarization changes were observed in 16 of 21 patients with CAD and in 19 of 60 patients with normal coronary arteries. With thallium scintigraphy, a reversible defect was observed in 19 of 22 patients with CAD and in 12 of 60 patients with normal coronary arteries. Regional wall motion abnormalities during dobutamine infusion developed in 18 of 22 patients with CAD and in none of the 62 patients with normal coronary arteries. All 3 tests had similar sensitivity for detection of CAD (76% for exercise treadmill test, 86% for thallium scintigraphy, and 82% for transesophageal dobutamine stress echocardiography). However, transesophageal dobutamine stress echocardiography had significantly higher specificity than the other 2 tests (100% vs 68% for exercise treadmill test and 80% for thallium scintigraphy; p = 0.0001). Thus, transesophageal dobutamine stress echocardiography is accurate for evaluation of CAD among women presenting with chest pain; its use should be considered when more conventional tests are equivocal or technically suboptimal.     

Results of a technique of pancreaticojejunostomy that optimizes blood supply to the pancreas

To evaluate whether the flow-mediated vasodilation and coronary flow reserve are impaired or not in patients with vasospastic angina (VA), we measured the changes of epicardial coronary artery diameter and flow reserve in spasm related-left anterior descending coronary artery (LAD). The flow mediated-response of epicardial coronary arteries in 15 VA were compared with 15 controls. Using quantitative coronary angiography, we measured the diameter of proximal (pLAD) and middle segment (mid-LAD) of LAD under baseline conditions, during increased blood flow after distal adenosine injection and after proximal administration of nitroglycerin. An increased fraction of average peak velocity after injection of adenosine was similar in both groups [control 340 (mean)+/-24 (SEM)%; VA 330+/-19%]. Flow-mediated vasodilation was preserved in all controls (pLAD 13.1+/-1.4%; mid-LAD 15.8+/-2.5%) but it was significantly impaired in patients with VA (pLAD -1.0+/-1.8%; mid-LAD 0.1+/-3.5%). The vasodilator response to nitroglycerin was comparable in controls (pLAD 25.8+/-2.8%; mid-LAD 27.2+/-2.8%) and VA (pLAD 26.2+/-5.2%; mid-LAD 26.7+/-3.5%). Coronary flow reserve is preserved in patients with VA. However, the flow-mediated response of spasm related-epicardial coronary artery is impaired. This may play an important role in the pathogenesis of coronary artery spasm.     

Non-cardiac chest pain: a real clinical problem

Non-cardiac chest pain is a frequent clinical problem. Between 10 and 50% of patients with anginal pain who are referred for arteriography are found to have normal coronary arteries. An oesophageal source of non-cardiac chest pain is reported in up to 60% of cases, most of which are attributable to gastro-oesophageal reflux disease. The exclusion of heart disease and the identification of an oesophageal origin of the pain may require an extensive work-up. The outcome in patients with non-cardiac chest pain is influenced by both the underlying diagnosis and the patient's perception of his or her symptom.