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At least 163 records · Page 9Linked to original sources
PubMed1989

Chest pain of esophageal origin.

Chest pain is a cause of significant anxiety in a patient. Even those who have no evidence of cardiac disease may have many visits to the emergency department and even repeated hospitalizations because of chest pain. Atypical chest pain is now the commonest reason for patients to be referred for esophageal manometry studies. The development of provocative studies has led both to an increased demonstration of esophageal origin of chest pain, as well as an increased awareness of the complexity of the esophageal response to a variety of stimuli. The possibility of a generalized smooth muscle disorder has been considered on the basis of studies demonstrating that many patients with microvascular angina have esophageal motor disorders. This review examines some of the issues related to the use of provocative agents to study patients with chest pain, in addition to briefly reviewing gastroesophageal reflux disease and esophageal mucosal disorders.

Chest Pain↗
PubMed1995

[Hypertensive cardiopathy. Studies on left ventricular hypertrophy].

This paper reviews the work of the cardiology Service of the Hospital de Basurto de Bilbao on hypertensive cardiomyopathy, diastolic disfunction and exercise tolerance, presenting a new pathophysiologic classification and the possibility of altering the underlying functional factors. The paper also reviews the presentation and evolution of microvascular angina in hypertensive patients.

Angina Pectoris↗
PubMed1995

Pathophysiology and management of noncardiac chest pain.

Noncardiac chest pain is a common but important clinical challenge with respect to diagnostic strategy as well as therapeutic intervention. The most common esophageal disorder associated with chest pain syndrome is gastroesophageal reflux; 24-hour ambulatory monitoring of esophageal pH and the determination of the symptom index are useful in patient evaluation. A high frequency of abnormal esophageal motility has been reported in noncardiac chest pain, but its clinical significance remains controversial. Patients with chest pain and normal coronary angiogram may have microvascular angina. Musculoskeletal conditions account for at least 10% of the cases of noncardiac chest pain. The potential effects of stress and altered psychological states in this phenomenon must be considered. The role of panic attacks in the production of pain needs to be clarified. Investigations to elucidate the exact cause of chest pain as well as its treatment should be individualized to the patient.

Arousal↗
PubMed1994

[Hyperinsulinemia and cardiovascular risk].

A large body of evidence has been accumulating that insulin plays a role in coronary heart disease (CHD). Hyperinsulinemia has been considered a risk factor for CHD according to prospective studies. Cross-sectional studies found an association between hyperinsulinemia and prevalence of CHD, while population studies have shown that populations at increased risk for CHD are hyperinsulinemic. Strong relations between hyperinsulinemia and atherosclerotic coronary lesions have been demonstrated by angiographic studies. It has recently been observed that also patients with microvascular angina are hyperinsulinemic. Several mechanisms have been proposed to explain the role of hyperinsulinemia in the development of atherothrombosis. Hyperinsulinemia is the consequence of insulin resistance, a defect in insulin-mediated glucose uptake. Experimental evidence suggests that insulin has actions that may promote atherosclerosis, which clinical studies suggest the existence of a metabolic syndrome characterized by the presence of major coronary risk factors in which insulin resistance is the common link.

Animals↗
PubMed1994

HRT mechanisms of action: carbohydrates.

Elevated insulin concentrations are frequently found in both men and women with coronary heart disease (CHD), and are likely to be due to insulin resistance. Hyperinsulinaemia may increase CHD risk by directly promoting atherogenesis, and insulin propeptides may also be important in this respect. However, increased insulin concentrations may adversely affect several other CHD risk factors, and it has been postulated that insulin resistance is a pivotal metabolic disturbance in a constellation of CHD risk factors. There is an association between hyperinsulinaemia and hypertension, although it is not known if this association is direct. Increased insulin concentrations are also associated with high triglycerides, low HDL or HDL2 concentrations, and increased small dense LDL. Obesity is also associated with insulin resistance, and it is the central or android body fat distribution which correlates with these metabolic disturbances. All these associated factors constitute a distinct syndrome--the insulin resistance syndrome--which is a frequent finding in patients with CHD, including microvascular angina. It is possible that the adverse associations of insulin resistance and dyslipidaemia are mediated through increased nonesterified fatty acid flux. Increased insulin levels are also associated with increases in the anti-fibrinolytic factor, plasminogen activator inhibitor-I (PAI-I). Whilst increased insulin levels are typically associated with insulin resistance, reduced hepatic insulin uptake may also be important. We now have techniques which can quantitate insulin secretion, hepatic uptake and release, elimination, and resistance. The menopause has appreciable effect on insulin and glucose metabolism. Estrogen and progesterone augment pancreatic insulin secretion, but the former reduces insulin resistance whilst the latter increases it.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1998

[In Process Citation]

Endothelium represents a large paracrine gland with an enormous reactive surface. By means of its numerous vasodilation and vasospastic factors it manages the basal and working tonus of vessels and thus also the regional flow and the access of target tissues to hormones and metabolic substrates. It manages also the proliferation and migration of myocytes of the vascular wall and thus its adaptation to overload. The dysfunctional states of endothelium are observed in arterial hypertensions, diabetes, dyslipoproteinaemia and they grow with age. They are the first stage of atherothrombogenic processes. They manifest themselves by a decreased vasodilation reserve of the vascular wall to strain, insulin and many other stimuli. On the contrary, quite frequently they paradoxically react to physical strain, acetylcholine, histamine, ATP etc. by vascular spasms which can determine vasospastic and microvascular angina pectoris including spasms and occlusions of e.g. coronary arteries in sites of insignificant stenoses with the origin of infarctions. The damaged endothelium, so to explain, conceives these stimuli in accordance with the encoded programme as a stimulus to the protection from haemorrhage during stress (fight or flight) and develops "suicidal" defensive reaction against them which we are nowadays able to modulate by administration of ACE-inhibitors, beta-blockers, hypolipidaemic drugs, inhibitors of cyclooxygenase-1 (30--100 mg of aspirin), Ca-antagonists and antioxidants including numerous nonpharmacological procedures. We can retard or halt the process of atherothrombogenesis and avoid or lower thus the number of sudden vascular ventricular as well as brain episodes, including the congestive heart failures, limb amputations and ischaemic damage of the brain. (Fig. 4, Ref. 70.).

Journal Article↗
PubMedDate not supplied

[Functions and dysfunctions of the vascular endothelium].

Endothelium represents a large paracrine gland with an enormous reactive surface. By means of its numerous vasodilation and vasospastic factors it manages the basal and working tonus of vessels and thus also the regional flow and the access of target tissues to hormones and metabolic substrates. It manages also the proliferation and migration of myocytes of the vascular wall and thus its adaptation to overload. The dysfunctional states of endothelium are observed in arterial hypertensions, diabetes, dyslipoproteinaemia, and they grow with age. They are the first stage of atherothrombogenic processes. They manifest themselves by a decreased vasodilation reserve of the vascular wall to strain, insulin and many other stimuli. On the contrary, quite frequently they paradoxically react to physical strain, acetylcholine, histamine, ATP etc. by vascular spasms which can determine vasospastic and microvascular angina pectoris including spasms and occlusions of e.g. coronary arteries in sites of insignificant stenoses with the origin of infarctions. The damaged endothelium, so to explain, conceives these stimuli in accordance with the encoded programme as a stimulus to the protection from haemorrhage during stress (fight or flight) and develops "suicidal" defensive reaction against them which we are nowadays able to modulate by administration of ACE-inhibitors, beta-blockers, hypolipidaemic drugs, inhibitors of cyclooxygenase-1 (30-100 mg of aspirin), Ca-antagonists and antioxidants including numerous non-pharmacological procedures. We can retard or halt the process of atherothrombogenesis and avoid or lower thus the number of sudden vascular ventricular as well as brain episodes, including the congestive heart failures, limb amputations and ischaemic damage of the brain. (Fig. 4, Ref. 70.)

Endothelium, Vascular↗
PubMed1997

A case of rest angina due to microvascular spasm.

A 66-year-old woman underwent elective cardiac catheterization for investigation of periodic attacks of chest pain at rest. During the examination, a chest pain attack occurred unexpectedly, resulting in ST elevation in the precordial leads on electrocardiography. Immediate coronary arteriography demonstrated no organic stenosis but markedly delayed contrast medium perfusion in the mild to distal portion of the left anterior descending artery. These phenomena spontaneously disappeared about 3 min later, and the patient was diagnosed as having angina pectoris due to microvascular spasm. The demonstration of angina pectoris due to microvascular spasm by coronary arteriography during a spontaneous attack is very rare.

Aged↗
PubMed1991

[Angina due to microvascular pathology].

Most ischemic heart disease in associated with severe coronary atherosclerosis. A small subset of patients, however, had angina pectoris despite angiographically normal coronary arteries and absence of inducible coronary spasm. Coronary microcirculation (i.e. arteries too small to be visualized by current angiographic techniques) has been identified as the weak point of these patients. Small coronary vessel involvement may be due to organic conditions (such as diabetes, vasculitis, systemic collagen-vascular diseases, infectious processes) that act through coronary thrombosis or embolism and related alteration in coronary vasomotion; alternatively, the vascular abnormality appears to be entirely functional (no ultrastructural myocardial changes) such as the case of hypertension, hypertrophic cardiomyopathy and syndrome X. Whatever the cause(s) and mechanism(s) of the small coronary artery involvement, this leads to myocardial ischemia and to the related complications as in classic atherosclerotic heart disease. Syndrome X is characterized by effort-induced angina pectoris, ST-segment changes during exercise testing, negative ergonovine test and reduced coronary reserve. A pre-arteriolar hypersensitivity to vasoconstrictor influences (elicited by cold pressor test or ergonovine) and a reduced vasodilator capacity (unmasked by metabolic and pharmacological studies) have been proposed as potential pathogenetic substrate. This dynamic alteration in vasomotion would answer for both symptoms and signs of myocardial ischemia, that, however, appear to be contemporarily elicitable in a minority of patients. Treatment with beta-blockers and calcium-antagonists has been found to be effective. The long-term follow-up shows favorable outcome with a high survival rate and a low incidence of cardiovascular events.

Angina Pectoris↗
PubMed1988

Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy.

When angina occurs in patients with hypertension, it is usually attributed to coronary artery disease or left ventricular hypertrophy. To determine the contribution of coronary microvascular abnormalities to angina in patients with hypertension, we evaluated hypertensive patients without coronary artery disease or left ventricular hypertrophy by measuring the coronary responses to rapid atrial pacing before and after administration of ergonovine. We compared 12 hypertensive patients who had pacing-induced angina with 13 normotensive subjects without such angina. The two groups had similar coronary flow (in the great cardiac vein) at rest; however, pacing increased coronary flow less in hypertensive patients with angina than in normotensive subjects (48 vs. 83 percent; P = 0.05). In the hypertensive patients with angina, pacing after ergonovine increased coronary flow by only 32 percent (as compared with 48 percent before ergonovine; P less than 0.05) and decreased coronary resistance by 15 percent (as compared with 28 percent before ergonovine; P less than 0.05), indicating the presence of ergonovine-induced vasoconstriction. In normotensive subjects, in contrast, cardiac pacing after ergonovine increased coronary flow by 112 percent (P less than 0.001), and its effect on coronary resistance was not different from that of pacing before ergonovine. The hypertensive patients with angina had a significant increase in myocardial oxygen extraction during pacing after ergonovine and less of an increase in myocardial lactate consumption - a response consistent with the presence of myocardial ischemia. Thus, angina in hypertensive patients without epicardial coronary disease may be caused by myocardial ischemia, which appears to be due to an abnormally elevated resistance of the coronary microvasculature.

Angina Pectoris↗
PubMed2000

Abnormal myocardial blood flow distribution in patients with angina pectoris and normal coronary arteriograms.

To evaluate coronary microvascular function and its relation to the genesis of chest pain and ST-segment depression during exercise in patients with syndrome X, pacing-induced changes in transmural myocardial blood flow distribution were quantitatively assessed by 2-dimensional myocardial contrast echocardiography. Of 25 patients with a history of chest pain and normal coronary arteries with the negative ergonovine test, 11 had exercise-induced chest pain and ST-segment depression (syndrome X), and 14 did not (controls). Myocardial blood flow distribution before and after pacing stress was assessed by measuring the ratio of the endocardial to epicardial gray level (ie, endo/epi gray level ratio) in the territory of the left anterior descending coronary artery. Pacing-induced chest pain and ST-segment depression were observed in syndrome X, but not in controls. The endo/epi gray level ratio in syndrome X significantly decreased after pacing (from 0.98+/-0.10 to 0.76+/-0.17, p<0.01), but not in controls (from 0.97+/-0.08 to 0.99+/-0.08, NS). Abnormal myocardial blood flow distribution may play an important role in exercise-induced chest pain and ST-segment depression in these patients.

Adult↗
PubMed1993

Evidence in support of the spasm of resistance vessel concept of ischemic heart disease: an update in 1993.

The goal of this communication is to provide more evidence for the ischemic heart disease (IHD) component of the spasm of resistance vessel (S-RV) concept of IHD and other ischemic diseases. The S-RV concept of IHD is considered to be an alternate paradigm which challenges the accepted understanding of this disorder. The theory asserts that primary S-RV directly induces symptoms in IHD, and this position is in opposition to the accepted view that symptoms are induced directly by primary occlusions of epicardial arteries by coronary artery disease, spasm, and thromboses. The theory, if valid, should be useful in reducing the impact of IHD, as it generally is accepted that the correct appreciation of basic pathophysiological mechanisms helps ensure the most appropriate prevention and treatment of disease.

Angina Pectoris↗
PubMed1999

Endothelial and metabolic characteristics of patients with angina and angiographically normal coronary arteries: comparison with subjects with insulin resistance syndrome and normal controls.

OBJECTIVES: This study was performed to characterize the endothelial and metabolic alterations of patients with angina and angiographically normal coronary arteries ("cardiac" syndrome X [CSX]) compared with subjects with insulin resistance syndrome ("metabolic" syndrome X [MSX]) and normal controls. BACKGROUND: Previous studies have found high endothelin-1 levels, impaired endothelium-dependent vasodilation and insulin resistance in patients with angina pectoris and angiographically normal coronary arteries. On the other hand, subjects with insulin resistance syndrome have shown high endothelin-1 levels. METHODS: Thirty-five subjects were studied: 13 patients with angina pectoris and angiographically normal coronary arteries (CSX group); 9 subjects with insulin resistance syndrome (MSX group) and 13 normal controls. All subjects received an acute intravenous bolus of insulin (0.1 U/kg) combined with a euglycemic clamp and forearm indirect calorimetry. Endothelin-1 levels, nitrite/nitrate (NOx) levels, end products of nitric oxide metabolism, glucose infusion rates (index of insulin sensitivity) and their incremental areas (deltaAUCs [area under curves]) were measured during this period. RESULTS: Basal endothelin-1 levels were higher in CSX and MSX groups than in normal controls (8.19 +/- 0.46 and 6.97 +/- 0.88 vs. 3.67 +/- 0.99 pg/ml; p < 0.01), while basal NOx levels were significantly higher in MSX group than in CSX and normal controls (36.5 +/- 4.0 vs. 24.2 +/- 3.3 and 26.8 +/- 3.2 mol/liter, p < 0.05). After insulin administration, the deltaAUCs of NOx (p < 0.05) were lower in CSX group than in MSX and normal controls, and the deltaAUCs of endothelin-1 were lower in group CSX than in normal controls. Glucose infusion rate was significantly lower in CSX and MSx groups than in normal controls (p < 0.01), suggesting that in both CSX and MSX groups insulin resistance is present. A positive correlation was found between the deltaAUCs of nitric oxide and the AUCs of glucose infusion rate. CONCLUSIONS: Blunted nitric oxide and endothelin responsiveness to intravenously infused insulin is a typical feature of patients with angina pectoris and angiographically normal coronary arteries and may contribute to the microvascular dysfunction observed in these subjects.

Calorimetry, Indirect↗