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At least 127 records · Page 7Linked to original sources
PubMed2004

Effect of oral L-arginine on blood pressure and symptoms and endothelial function in patients with systemic hypertension, positive exercise tests, and normal coronary arteries.

Thirteen hypertensive patients with microvascular angina were studied before and after receiving oral L-arginine (4 weeks, 2 g, 3 times daily). L-arginine significantly improved angina class, systolic blood pressure at rest, and quality of life. Maximal forearm blood flow, plasma L-arginine, L-arginine:asymmetric dimethyl arginine ratio, and cyclic guanylate monophosphate increased significantly after treatment. In medically treated hypertensive patients with micro-vascular angina, oral L-arginine may represent a useful therapeutic option.

Administration, Oral↗
PubMed2005

Are low total serum antioxidant status and elevated levels of C-reactive protein and monocyte chemotactic protein-1 associated with cardiac syndrome X?

BACKGROUND: Cardiac syndrome X, also known as microvascular angina, is characterized by exercise-induced chest pain occurring despite a normal coronary angiogram. Several causes and mechanisms have been proposed to explain both the chest pain and ST segment depression. In this study, the association, if any, between cardiac syndrome X and several factors, including blood total antioxidant status, C-reactive protein (CRP), and monocyte chemotactic protein-1 (MCP-1) levels, was investigated. METHODS AND RESULTS: The study group comprised 36 patients who had been diagnosed as cardiac syndrome X on the basis of a positive treadmill test and a normal coronary angiogram, and 24 control patients. Total serum antioxidant status and CRP were assessed, and the levels of P-selectin, MCP-1, and interleukins 6 and 10 were also measured. Total serum antioxidant levels were determined to be significantly lower in the cardiac syndrome X patients than in the controls. CRP and serum MCP-1 levels, however, were found to be significantly higher in the cardiac syndrome X group. The total serum antioxidant levels and serum MCP-1 levels were comparable with the levels observed in a group of chronic stable angina patients. CONCLUSIONS: In the present study, patients who had been diagnosed as cardiac syndrome X demonstrated increased systemic oxidative and enhanced inflammatory status.

Aged↗
PubMed1993

Chest pain and angiographically normal coronary arteries. Implications for treatment.

Approximately 20% to 30% of patients who undergo coronary arteriography for the evaluation of chest pain are found to have normal coronary arteries. These patients have a survival rate comparable to that of the normal population, yet they continue to complain of symptoms on extended follow-up, and about half of this group are disabled on account of chest pain. Once other clinically obvious disorders have been ruled out, common diagnostic considerations include microvascular angina, esophageal dysfunction, and perhaps fibromyalgia. Panic disorder, however, is the most common condition affecting these patients and can be diagnosed in at least one third of the group, with or without the presence of the other conditions mentioned. Appropriate diagnosis and treatment can reduce the psychosocial morbidity so frequently seen in these patients.

Chest Pain↗
PubMed1999

[Insulin resistance and the coronary syndrome].

The different diseases associated with the insulin resistance syndrome--diabetes mellitus or impaired carbohydrate tolerance, atherogenic lipoprotein phenotype, arterial hypertension and central type of obesity are the main risk factors of atherosclerosis. The reduced sensitivity of target tissues to the metabolic action of insulin (insulin resistance) is considered at present a separate risk factor. The authors analyze on the basis of a group of 210 coronarographic patients the influence of insulin resistance and associated etiopathogenetic risk factors on coronary lesions evaluated by the method of quantitative coronarography. From the results of the investigation ensues that insulin resistance is the most frequent metabolic deviation in patients with coronary disease whereby in the macrovascular group it was found in 74.3% and in the group with microvascular angina pectoris in 64.3% of the patients. Changes in the lipoprotein spectrum were a more frequent and earlier manifestation of insulin resistance than impaired carbohydrate metabolism. The change from functional changes of the vascular wall (impaired endothelium-dependent vasodilatation) to the development of an atheromatous plaque depends on the total number of cholesterol conveying lipoproteins assessed by means of the apoprotein B level and on the capacity of the reverse cholesterol transport, whereby both mechanisms are greatly influenced by insulin sensitivity. The degree of coronary affection evaluated by means of a coronary score, is in patients with manifest diabetes comparable with the affection in patients with insulin resistance without manifest diabetes and these two groups differ very significantly as to the extent and degree of affection from patients with a normal sensitivity to the effect of insulin.

Coronary Angiography↗
PubMedDate not supplied

[Positive exercise test and normal exercise myocardial perfusion SPECT. Clinical significance].

OBJECTIVE: To establish, in our area, the clinical significance of a normal exercise myocardial perfusion study, in patients with an ischemic response of the exercise test. MATERIAL AND METHODS: A retrospective study was carried out in our Service for the last four years. We studied 45 patients (41 women and 4 men) with an ischemic response of the exercise test and normal myocardial perfusion SPECT, during a mean follow-up of 13,2 months. We considered the final clinical diagnosis according to clinical evolution, therapy outcome and coronary angiography results. RESULTS: The presence of positive exercise test and normal SPECT was predominant in women (93.3%). In 35 patients (77.8%), the final diagnosis was chest pain of probable non-coronary origin (not secondary to coronary artery disease): 18 patients were diagnosed of hypertensive cardiomyopathy, 3 of valvulopathy, 2 of vasospastic angina, 1 of hypertrophic obstructive cardiomyopathy, 1 of microvascular angina, 1 of angina due to arrhythmia, and 9 patients diagnosed of atypical chest pain due to functional or non-cardiac origin. In 10 patients (22.2%), the final diagnosis was chest pain of probable coronary origin. We did not observe any major cardiac events (cardiac death and nonfatal myocardial infarction) during the follow-up period. CONCLUSIONS: Patients with chest pain, positive exercise test and normal SPECT have an excellent prognosis within an intermediate follow-up period. 77.8% of patients were diagnosed of chest pain of non-coronary origin. The most common cause of non-coronary chest pain was hypertensive cardiomyopathy (51.4%), followed by functional or non-cardiac chest pain (28.6%).

Aged↗
PubMed1999

Coronary microvascular disease in humans.

Myocardial perfusion abnormalities occur in the absence of epicardial coronary artery disease in patients with a wide spectrum of cardiovascular disorders including microvascular angina, hypertension and left ventricular hypertrophy, coronary atherosclerosis, hypercholesterolemia, and non-ischemic left ventricular dysfunction. These patients have limited coronary microvascular dilator reserve which occasionally is associated with evidence of myocardial ischemia. Primary microvascular hyperconstriction (spasm) is also proposed to cause myocardial ischemia in a subset of patients with rest angina. There is ample evidence suggesting that endothelial dysfunction contributes to microvascular dysfunction, but the precise mechanism of endothelial dysfunction is not known. Nitric oxide is one of the key molecules which control microvascular tone and therefore coronary blood flow, and its decreased availability appears to be involved under certain conditions. This hypothesis has attracted considerable interest as a new therapeutic strategy for these patients having coronary microvascular derangements caused by divergent cardiovascular diseases.

Angina Pectoris↗
PubMed1992

Critique of the session on diagnostic testing.

During the session on diagnostic testing, various diagnostic tests used to identify the cause of chest pain were discussed. This critique of diagnostic assessments of the complex etiology of chest pain is presented as a contribution toward further investigation and clarification of this difficult clinical syndrome. The first step in the evaluation process is to exclude coronary artery disease. Patients with angina and normal coronary artery flow may have atypical disease, such as microvascular angina or syndrome X. The precise relationship between these disorders and esophageal disease or gastroesophageal reflux, as well as their possible involvement in chest pain of undetermined origin, requires further definition. A limitation of esophageal provocation tests is that they may identify the esophagus as the source of pain without determining the specific esophageal disorder that causes the pain. Problems associated with 24-hour pH and pressure monitoring include (a) poor correlation between reflux episodes and heartburn symptoms, (b) the lack of a good functioning swallowing signal, and (c) the huge amount of data that must be analyzed, along with shortcomings in computer-aided analysis. Nevertheless, the various available diagnostic tests can provide important information to the clinician.

Angina Pectoris↗
PubMed1991

Evidence of endothelial dysfunction in coronary resistance vessels in patients with angina pectoris and normal coronary angiograms.

This study determines whether an impaired endothelium-mediated vasodilation in coronary resistance vessels exists in patients with microvascular angina. In 23 patients with clinically suspected coronary artery disease and smooth coronary arteries in the angiogram, coronary flow in response to an endothelium-related (acetylcholine) and endothelium-unrelated (dipyridamole) vasodilation was measured. Coronary flow was determined by the gas-chromatographic argon method (1) before, (2) with intracoronary acetylcholine infusion, and (3) after dipyridamole administered intravenously. In 8 patients, acetylcholine did not significantly increase coronary flow (from 91 +/- 28 to 118 +/- 37 ml/min.100 g), whereas flow was greatly increased after administration of dipyridamole (258 +/- 97 ml/min.100 g), indicating an endothelium-related vasodilator defect. In 6 patients, neither acetylcholine nor dipyridamole caused a significant increase in coronary flow, indicating an impaired coronary vasodilation on the vascular site. In 6 patients, coronary flow increased markedly after both administration of both acetylcholine and dipyridamole (from 81 +/- 26 to 191 +/- 68 and 234 +/- 87 ml/min.100 g). In 3 patients given acetylcholine, coronary artery constriction occurred. No significant correlation was found between the response to acetylcholine and that to dipyridamole (r = 0.40, p = not significant). The results indicate that in a subgroup of patients with smooth coronary arteries angina can be caused by an abnormality of the endothelial function in the microcirculation.

Acetylcholine↗
PubMed1993

Evidence of impaired endothelium-dependent coronary vasodilatation in patients with angina pectoris and normal coronary angiograms.

BACKGROUND: A group of patients has been described who have chest pain resembling angina and positive exercise tests, but normal coronary angiograms and no coronary-artery spasm. This constellation of features has sometimes been called syndrome X or microvascular angina. We attempted to determine whether endothelium-dependent vasodilatation of the coronary vasculature was impaired in patients with this syndrome. METHODS: We infused the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilators papaverine and isosorbide dinitrate into the left coronary artery of 9 patients and 10 control subjects. The diameter of the left anterior descending coronary artery was assessed by quantitative angiography, and changes in coronary blood flow were estimated with the use of an intracoronary Doppler catheter. RESULTS: Acetylcholine, given in doses of 1, 3, 10, and 30 micrograms per minute, increased coronary blood flow in a dose-dependent manner in both groups. However, the mean (+/- SD) acetylcholine-induced increases in coronary blood flow were significantly less (P < 0.001) in the patient (8 +/- 14, 37 +/- 37, 59 +/- 67, and 103 +/- 77 percent, respectively) than in the controls (62 +/- 52, 186 +/- 93, 341 +/- 128, and 345 +/- 78 percent, respectively). The changes in coronary blood flow in response to 2 mg of isosorbide dinitrate (236 +/- 66 percent vs. 280 +/- 56 percent) and 10 mg of papaverine (366 +/- 168 percent vs. 411 +/- 92 percent) did not differ significantly between the patients and controls. The administration of papaverine resulted in myocardial lactate production in the patients but not in the controls. The three lower doses of acetylcholine caused a similar degree of dilatation of the left anterior descending coronary artery in the two groups, and the highest dose caused a similar degree of constriction in the two groups. Isosorbide dinitrate and papaverine caused a similar degree of dilatation in both groups. CONCLUSIONS: These findings suggest that endothelium-dependent dilatation of the resistance coronary arteries is defective in patients with anginal chest pain and normal coronary arteries, which may contribute to the altered regulation of myocardial perfusion in these patients.

Acetylcholine↗
PubMed2000

The relationship of oxidized lipids to coronary artery stenosis.

A total of 1200 patients with angina were cardiac catheterized establishing that 63% had 70-100% stenosis, 12% had 10-69% stenosis of one or more of their coronary arteries and 25% had microvascular angina listed as 0% stenosis. Prior to catheterization 10 ml of blood was drawn and the plasma subjected to analysis for the concentration of cholesterol, lipid peroxides (LPX), total antioxidant capacity (TAOC), fibrinogen (FB), ceruloplasmin (CP) and activation of polymorphonuclear leukocytes (PMNLs). Comparisons were made to non-smoking controls without angina. Significant differences in LPX were found between the patients with 0 and 10-69% stenosis (P<0.001), with 10-69 and 70-100% stenosis (P<0.001), and with 0 and 70-100% stenosis (P<0.001). Under 70 years of age there was a significant difference in LPX between patients with all levels of stenosis and age and sex matched controls (P<0.001). Differences in the mean plasma cholesterol concentration for different levels in the degree of stenosis were not significant, indicating that LPX provided consistent data on the severity of stenosis while the plasma cholesterol concentration did not. Compared with controls an increase in activation of PMNLs (P<0.01), an increase in concentration of both FB and CP (P<0.01) and a decrease in total antioxidant capacity were noted in the plasma of catheterized patients. In summary the concentration of oxidation products rather than the concentration of cholesterol in the plasma identified stenosis in cardiac catheterized patients.

Adult↗
PubMed2005

Clinical implications of assessing coronary flow velocity reserve and plasma endothelin-1 in hypertensive patients.

Previous reports have indicated that hypertensive patients who have angina-like chest pain and normal coronary arteriograms have reduced coronary flow velocity reserve (CFVR) levels. In addition, elevated plasma endothelin-1 (ET-1) levels have been reported to be associated with microvascular angina. The purpose of this study was to evaluate the plasma ET-1 levels and CFVR in patients with chest pain but without coronary artery disease (CAD). A total of 66 patients were included in this study. CAD was ruled out by exercise stress test or coronary angiogram. Plasma ET-1 and CFVR measurements were performed in patients with (n=35) and without (n=31) a history of angina-like chest pain. CFVR was measured using adenosine-triphosphate stress transthoracic Doppler echocardiography. The mean ET-1 level was significantly higher and the CFVR was significantly lower in patients in the symptomatic group than in those in the asymptomatic group (ET-1: 3.85 +/- 1.24 pg/ml vs. 2.98 +/- 1.27 pg/ml, CFVR: 2.26 +/- 0.48 vs. 2.77 +/- 0.11, respectively). Plasma ET-1 level and CFVR were significantly correlated with each other (-r = 0.265, p = 0.033). Age, blood pressure, cardiovascular risk factors, and left ventricular mass index were similar between the two groups. The results of multiple regression analysis indicate that age (p = 0.008) and plasma ET-1 concentration (p = 0.031) had statistically independent associations with CFVR. Attenuated CFVR in the symptomatic hypertensive patients was associated with endothelial dysfunction, which results in elevated plasma ET-1 levels. The link between these two parameters may play a role in the genesis of chest pain in hypertensive patients without CAD.

Aged↗
PubMed1992

Coronary haemodynamics in hypertensive heart disease.

Cardiac constituents affected in arterial hypertension comprise the myocardium, interstitium and coronary circulation. With regard to coronary circulation, arterial hypertension is an important risk factor in coronary artery disease, but even in the absence of coronary artery disease, hypertensive patients frequently have angina pectoris or reveal electrocardiographic abnormalities suggestive of myocardial ischaemia due to coronary insufficiency. Under clinical conditions, determination of coronary flow reserve (dipyridamole; Argon-method) allows for the evaluation of impairment of coronary regulatory reserve. In comparison to healthy normotensives, coronary haemodynamics in hypertensive patients with microvascular angina are characterized by a severely increased minimal coronary resistance and reduced maximal coronary blood flow to dipyridamole. Accordingly, coronary reserve is markedly reduced by about 40%, and metabolic, myocardial and vascular factors may be involved in this reduction. In the compensated stage of arterial hypertension, with concentric left ventricular hypertrophy, myocardial factors, such as myocyte hypertrophy, extravascular compressing forces and functional implications of impaired relaxation, as well as metabolic factors, contribute to impairment in coronary reserve to a minor extent. The reduction in coronary flow reserve is not proportional to the elevation in left ventricular muscle mass and thus the degree of left ventricular hypertrophy does not seem to determine the reduction in vasodilator reserve directly. Thus the reduction in coronary reserve seems to be primarily the consequence of an impaired vasodilating capacity of the coronary resistance vessels, as indicated by a severely increased minimum coronary resistance to dipyridamole, i.e. a severely reduced overall coronary conductance capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed2006

Frequency and severity of myocardial perfusion abnormalities using Tc-99m MIBI SPECT in cardiac syndrome X.

BACKGROUND: Cardiac syndrome X is defined by a typical angina pectoris with normal or near normal (stenosis <40%) coronary angiogram with or without electrocardiogram (ECG) change or atypical angina pectoris with normal or near normal coronary angiogram plus a positive none-invasive test (exercise tolerance test or myocardial perfusion scan) with or without ECG change. Studies with myocardial perfusion imaging on this syndrome have indicated some abnormal perfusion scan. We evaluated the role of myocardial perfusion imaging (MPI) and also the severity and extent of perfusion abnormality using Tc-99m MIBI Single Photon Emission Computed Tomography (SPECT) in these patients. METHODS: The study group consisted of 36 patients with cardiac syndrome X. The semiquantitative perfusion analysis was performed using exercise Tc-99m MIBI SPECT. The MPI results were analyzed by the number, location and severity of perfusion defects. RESULTS: Abnormal perfusion defects were detected in 13 (36.10%) cases, while the remaining 23 (63.90%) had normal cardiac imaging. Five of 13 (38.4%) abnormal studies showed multiple perfusion defects. The defects were localized in the apex in 3, apical segments in 4, midventricular segments in 12 and basal segments in 6 cases. Fourteen (56%) of all abnormal segments revealed mild, 7(28%) moderate and 4 (16%) severe reduction of tracer uptake. No fixed defects were identified. The vessel territories were approximately the same in all subjects. The Exercise treadmill test (ETT) was positive in 25(69%) and negative in 11(30%) patients. There was no consistent pattern as related to the extent of MPI defects or exercise test results. CONCLUSION: Our study suggests that multiple perfusion abnormalities with different levels of severity are common in cardiac syndrome X, with more than 30 % of these patients having at least one abnormal perfusion segment. Our findings suggest that in these patients microvascular angina is probably more common than is generally believed.

Journal Article↗
PubMed1998

[Improved coronary vasodilator capacity by drug lipid lowering therapy in patients in the early stage of coronary atherosclerosis with reduced coronary reserves and moderate LDL hypercholesteremia].

BACKGROUND: An abnormal coronary flow reserve represents an early marker of impaired blood flow regulation in the natural history of coronary atherosclerosis under the impact of risk factors such as hypercholesterolemia. Our clinical investigation was aimed at assessing noninvasively the integrative coronary flow response to dipyridamole stress in 18 consecutive patients with microvascular angina, only moderately elevated LDL-cholesterol levels (168 +/- 33 mg/dl), and reduced vasodilator capacity despite normal (n = 9) or slightly abnormal (n = 9) coronary arteriograms (minimal disease with luminal irregularities and/or diameter reduction < or = 30%) before and after 6-month lipid-lowering therapy (simvastatin). METHODS: Regional and averaged myocardial blood flow were measured at rest and after dipyridamole induced vasodilation (0.56 mg/kg) using dynamic positron emission tomography (PET) and N-13 ammonia as flow tracer related to a 3-compartment kinetic model. Baseline data (mean +/- SD): 13 males, 5 females; mean age: 56 +/- 8 years; basal coronary flow: 90 +/- 22 ml/min x 100 g; after lipid intervention: 93 +/- 18 ml/min x 100 g (n.s.). Total cholesterol: 246 +/- 45 mg/dl. RESULTS AFTER 6-MONTH LIPID INTERVENTION: Total cholesterol decreased to 170 +/- 36 mg/dl (p < 0.001); mean LDL level: 97 +/- 26 mg/dl (p < 0.001). Coronary dilator capacity increased, assessed in terms of minimal coronary resistance: 0.38 +/- 0.08 vs 0.49 +/- 0.09 units at baseline (p < 0.01), myocardial blood flow under dipyridamole: 232 +/- 43 vs 186 +/- 37 ml/min x 100 g at baseline (p < 0.01), and instantaneous flow ratio: 2.6 +/- 0.7 vs 2.2 +/- 0.6 (p = 0.06). Concomitantly, a considerable regression of angina was noticed in the majority of patients. CONCLUSIONS: An improvement of the non-invasively determined integrative dipyridamole induced coronary vasodilator capacity may be achieved after 6 months by intensive lipid lowering at a very early stage of coronary atherosclerosis. Consequently, aggressive cholesterol-lowering therapy represents an antiischemic and antianginal approach suggesting, at least in part, functional reversal and probably prevention of further disease progression.

Adult↗
PubMed1992

Chest pain of undetermined origin: overview of pathophysiology.

Patients with unexplained chest pain represent a major clinical dilemma for primary-care physicians, gastroenterologists, and cardiologists. References to this prevalent clinical problem date to more than 150 years ago; confusion about its pathophysiology has resulted in the use of a variety of descriptive terms such as "noncardiac," "atypical," and "angiographically negative" chest pain. Since none of these terms applies to all cases, the description "chest pain of undetermined origin" may be preferable. Because the esophagus has a similar location and innervation as the heart, an esophageal source for unexplained chest pain syndromes has been frequently suggested. Recent studies have emphasized the importance of gastroesophageal reflux as a likely component of esophageal pain. Moreover, "irritable esophagus" is an emerging concept that implies a generalized alteration in esophageal pain threshold, that is, abnormal nociception. The potential effects of stress or altered psychological states in this phenomenon must be considered, and the role of "panic attacks" in the production of pain in these patients needs to be clarified. In addition, stress may produce altered esophageal motility and lead to manometric abnormalities such as the "nutcracker esophagus" or a hypertensive lower esophageal sphincter. Finally, the precise contribution of the heart in producing pain in patients with normal coronary angiograms remains unclear because the precise role of microvascular angina has yet to be clarified.

Angina Pectoris↗
PubMed1992

Overview of diagnostic testing for chest pain of unknown origin.

Identifying the cause of recurrent chest pain may be difficult. Significant coronary artery disease must be excluded before patients can be assured that their symptoms are truly "noncardiac." A normal coronary angiogram is the most definitive test but this may not preclude the presence of a new "fly in the ointment," i.e., microvascular angina. Musculoskeletal pain syndromes, psychological problems, and esophageal disorders, including both esophageal motility disorders and gastroesophageal reflux disease, are the most common causes of noncardiac chest pain. Nearly 30% of these patients will have an esophageal motility disorder, although its clinical relevance in the asymptomatic patient is controversial. Simple, inexpensive, provocation tests (most commonly edrophonium, bethanechol, and/or balloon distention) have been developed to recreate motility-related chest pain in the laboratory. These tests can identify the esophagus as the source of pain, but in most cases they do not direct therapy. Other disadvantages of provocation tests include the lack of a gold standard reference point, side effects, and the need for placebo because of a subjective end point. Recently, ambulatory esophageal pH and pressure monitoring have been used to define precisely the cause of esophageal chest pain. These systems can record multiple episodes of pain for up to 24 hours in an outpatient setting and have shown that gastroesophageal reflux (rather than motility disorders) is the most common esophageal cause of pain. However, these studies also suggest that many episodes of chest pain do not have an identifiable esophageal cause. Furthermore, this equipment is expensive, uncomfortable, may alter normal activity, and is not useful in patients having infrequent pain episodes. Psychological disturbances should be carefully sought in any patient with noncardiac chest pain: Many patients have anxiety, depression, or panic attacks that may complicate or contribute to their reported symptoms. It is questionable if these patients need additional testing. Rather, the challenge of the future is to prove that the multitude of tests aid in the overall treatment and outcome of patients with noncardiac chest pain.

Angina Pectoris↗
PubMed1992

Provocation testing in noncardiac chest pain.

The ability to reproduce chest pain and to identify the esophagus as the source of this pain are the major reasons why provocation testing has become standard in the evaluation of patients with noncardiac chest pain. Recent studies that challenge the validity of performing provocation tests have polarized experts into two camps: those who would abandon such testing because of its low sensitivity and low specificity, and those who would use testing judiciously because of moderate increases in diagnostic yield. Use of 24-hour pH and pressure testing has shown a high number of chest pain events associated with acid reflux in patients with positive cholinergic stimulation tests and esophageal dysmotility, as well as pain with esophageal dysmotility in patients with positive acid infusion tests. Mechanisms of esophageal chest pain are not known. All provocation agents can decrease coronary flow reserve (i.e., induce microvascular angina), thus raising the question of a cardiac source of pain even in patients with positive presumed esophageal provocation. Acid infusion, cholinergic stimulation, and balloon distention are discussed in light of 24-hour pH and pressure monitoring. Esophageal distention and the role of acid in inducing chest pain are emphasized. The role of stress, the use of defined stressors to induce chest pain, and altered pain perception as a final common pathway for chest pain are examined.

Chest Pain↗