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Cardiac syndrome X

See microvascular angina

See Coronary microvascular dysfunction causing cardiac ischemia in women

Cardiac syndrome X (CSX) is typical anginalike chest pain with evidence of myocardial ischemia in the absence of flow-limiting stenosis on coronary angiography.

Approximately 20%-30% of patients undergoing coronary angiography for evaluation of anginalike chest pain may have nonobstructive coronary artery disease.

It is characterized by a decrease in coronary flow reserve without epicardial artery stenosis, microvascular angina.

It is a clinical and pathophysiological heterogeneous process.

Its more common in women than in men.

It frequently occurs in perimenopausal and postmenopausal women.

Individuals with cardiac syndrome X are typically younger than those with angina due to obstructive coronary artery disease.

Mechanisms proposed: cardiac syndrome:

Endothelial dysfunction (microvascular angina)

Myocardial ischemia

Insulin resistance

Abnormal autonomic control

Altered cardiac sensitivity

Estrogen deficiency

Endothelial dysfunction

Endothelial dysfunction in cardiac syndrome X is linked to risk factors such as smoking, obesity, hypercholesterolemia, and inflammation.

Low levels of high-density lipoprotein cholesterol (HDL-C) is associated with systemic inflammation in cardiac syndrome X.

Cardiac syndrome X also associated with elevated plasma C-reactive protein levels, correlating with disease activity and endothelial dysfunction.

The findings of endothelial dysfunction, reduced bioavailability of endogenous nitric oxide and increased plasma levels of endothelin-1 may account, for the abnormal coronary microvasculature in cardiac syndrome X.

Several studies support the presence of hyperinsulinemia in cardiac syndrome X.

Individuals with cardiac X syndrome may manifest difficulties with motor control or with mathematics.

Metformin has been shown to improve vascular function and decrease myocardial ischemia in nondiabetic women with chest pain and angiographically normal coronary arteries.

Autonomic nervous system abnormalities characterized by adrenergic hyperactivity and baroreceptor dysfunction have been demonstrated in several studies.

Studies have suggested that abnormalities in pain perception may be the principal abnormality in patients with chest pain and normal findings on coronary angiography.

An altered central neural handling of afferent signals may contribute to the abnormal pain perception in patients with cardiac syndrome X.

Estrogen deficiency frequently occurs in perimenopausal or postmenopausal women with cardiac syndrome X.

In postmenopausal women with cardiac syndrome X, estrogen replacement therapy improves coronary endothelial function, decreases anginal frequency, and improves exercise-induced angina.

Endothelial dysfunction in cardiac syndrome X is linked to risk factors such as smoking, obesity, hypercholesterolemia, and inflammation.

Low levels of HDL-C appears to be associated with systemic inflammation in cardiac syndrome X.

Elevated plasma C-reactive protein levels, a marker of inflammation, have been shown to correlate with disease activity and endothelial dysfunction.

Endothelial dysfunction is associated with reduced bioavailability of endogenous nitric oxide and increased plasma levels of endothelin-1 (ET-1).

The presence of hyperinsulinemia has been noted in many patients with cardiac syndrome X, and metformin has been shown to improve vascular function and decrease myocardial ischemia in nondiabetic women with chest pain and angiographically normal coronary arteries.

Autonomic nervous system irregularities characterized by adrenergic hyperactivity and baroreceptor dysfunction has been demonstrated.

Improvement of coronary flow reserve by α-adrenergic blockade with doxazosin has been shown in cardiac X syndrome.

Abnormalities in pain perception due to altered central neural afferent signaling may be the principal abnormality in patients with chest pain and normal findings on coronary angiography.

It frequently occurs in perimenopausal or postmenopausal women, supporting a role for estrogen deficiency.

In postmenopausal women with cardiac syndrome X, estrogen replacement improves coronary endothelial function, decreases anginal frequency, and improves exercise-induced angina.

Patients with cardiac syndrome X, have an excellent prognosis.

There is an increased coronary atherosclerotic burden at 10-year in women with cardiac syndrome X who displayed coronary endothelial dysfunction.

In The Women’s Ischemic Syndrome Evaluation study of middle-aged women with cardiac syndrome X, showed that these patients often have atherosclerosis on intravascular coronary ultrasound and face a 2.5% annual rate adverse cardiac events.

Approximately 59%of patients with cardiac syndrome X have anginalike chest pain.

The remainder of patients with cardiac X syndrome have atypical chest pain.

The duration of anginal-type chest pain in cardiac X syndrome is often prolonged.

Cardiac X syndrome anginal pain often does not respond to sublingual nitroglycerin.

A significant proportion of patients in whom cardiac syndrome X is diagnosed may have a noncardiac etiology for their chest discomfort: fibromyalgia, esophageal dysfunction, costochondritis.

Abnormal physical findings are uncommon in cardiac syndrome X.

The resting ECG findings may be normal.

Nonspecific ST-T–wave abnormalities are often observed, sometimes in association with the chest pain.

Approximately 20% of patients with cardiac syndrome X have positive results on exercise tests.

Left ventricular function is usually normal at rest and during stress.

Computed tomography coronary angiography, positron emission tomography, and cardiovascular magnetic resonance imaging may become part of the diagnostic algorithm.

Tests to evaluate endothelial function is an invasive determination of coronary flow reserve via Doppler guidewire in the cardiac catheterization laboratory.

It quantifies coronary blood flow in response to nitroglycerine and acetylcholine infusion.

Myocardial ischemia secondary to abnormal coronary reactivity testing can be detected noninvasively via single photon emission computed tomography, positron emission testing, and stress cardiac magnetic resonance imaging: the sensitivity and specificity of these measures remain incompletely understood.

Medical care of cardiac syndrome X (CSX) is treated with: lifestyle modification, diet, exercise, smoking cessation, and weight reduction, use of anti-anginal, anti-atherosclerotic, and anti-ischemic agents.

Spinal cord stimulation can reduce chest pain and improved quality of life in about 50% of patients resistant to all other treatment.

Cognitive behavioral therapy shows promising results in reducing episodes of chest discomfort over a period of 3-6 months.

Physical training program may improve exercise capacity and reduce the frequency of chest pain episodes.

Enhanced external counter pulsation may reduce symptoms through an improvement in endothelial function, promotion of collateralization, ventricular function enhancement, and peripheral effects resembling those seen with regular physical exercise.

Beta blockers seem to be most effective in reducing the frequency and severity of angina and in improving exercise tolerance.

Pharmacodynamic consequences of beta1 -receptor blockade include decreases in (1) resting and exercise heart rate, (2) cardiac output, and (3) systolic and diastolic blood pressure.

Beta blockers have a negative chronotropic effect that decreases the heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, reduction of sympathetic outflow from the central nervous system (CNS), and suppression of renin release from the kidneys.

Angiotensin-converting enzyme (ACE) mechanism of action is thought to be from increased bioavailability of nitric oxide and improvement in endothelial function.

Statins improve the exercise tolerance, time to electrocardiographic changes on stress testing, and brachial artery flow.

Hormone therapy may be beneficial in postmenopausal women, reducing the frequency of anginal episodes.

Estrogen may act by improving endothelial coronary vasomotion.

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