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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The existence of coronary endoarterial cushions (CEC) in the human heart as nonpathological, functional entities has been debated, and CEC have been sparsely reported in animals. Arterial cushions are localized thickenings that protrude into the lumen of specific arteries. We have identified CEC in the rhesus monkey, dog, sheep, goat, pig, rabbit and rat, and in the human heart. Two distinct types are described: the ovoid CEC arranged singly, in pairs, or in groups of three to four, and the less common polypoid CEC seen primarily in humans. The highest incidence of CEC in rabbits and humans was in the left ventricle in arteries 150-488 microns in diameter. Light and electron microscopy demonstrated intimal location with smooth muscle cells surrounded by ground substance, collagen and elastin fibers in a highly organized pattern. Nerve fibers identified by their immunoreactivity with antiserum to the vasodilatory calcitonin-gene-related peptide contacted the CEC along the tunica media and were occasionally seen within CEC. Arrangement and histological composition of CEC suggest a role in the regulation of local blood flow and myocardial perfusion. In human hearts, the CEC density index correlated highly with the degree of heart disease. In subjects with high heart disease rating, increased connective tissue, lipid-like infiltration and calcification was seen within CEC, and foam cells were present in CEC of obese rabbits. This suggests that CEC in coronary arteries could be predisposed sites of atherosclerosis, and that injured CEC can cause coronary artery spasm and ischemia. We conclude that CEC occur in animals and humans as innervated intimal smooth muscle cushions that might have a role in myocardial perfusion and heart disease.
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PMID:Intramyocardial arterial cushions of coronary vessels in animals and humans: morphology, occurrence and relation to heart disease. 892 19

This study examines the incidence of spasm by intracoronary injection of acetylcholine in Japanese patients who underwent coronary angiography. The subjects were 685 consecutive patients (477 men, mean age 63.2 +/- 7.5 years) who were studied with an acetylcholine test. Acetylcholine was injected in incremental doses of 20, 50, and 80 microg into the right coronary artery and 20, 50, and 100 microg into the left coronary artery. Spasm was defined as total or subtotal occlusion. Coronary vasospasm was determined in 221 patients (32.3%). Spasm occurred often during effort and rest in patients with angina (25 of 51, 49.0%), exertional angina (25 of 74, 33.8%), recent myocardial infarction (30 of 80, 37.5%), healed myocardial infarction (14 of 37, 37.8%), and especially in patients with rest angina (83 of 124, 66.9%), whereas spasm was relatively uncommon in patients with nonischemic heart disease (23 of 252, 9.1%). Spasm was superimposed on significant atherosclerotic lesions in 35.9% of patients as well as on nonfixed atherosclerotic lesions in 30.8% of patients. We conclude that >9% of Japanese patients may have coronary vasospasm with intracoronary injection of acetylcholine and recommend the provocation test for evaluating coronary vasospasm if coronary angiography is undertaken.
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PMID:Frequency of provoked coronary vasospasm in patients undergoing coronary arteriography with spasm provocation test of acetylcholine. 1021 81

Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
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PMID:Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder. 1524 Apr 8

During voluntary hyperventilation in unanesthetized humans, hypocapnia causes coronary vasoconstriction and decreased oxygen (O(2)) supply and availability to the heart. This can induce local epicardial coronary artery spasm in susceptible patients. Its diagnostic potential for detection of early heart disease is unclear. This is because such hypocapnia produces an inconsistent and irreproducible effect on electrocardiogram (ECG) in healthy subjects. To resolve this inconsistency, we have applied two new experimental techniques in normal, healthy subjects to measure the effects of hypocapnia on their ECG: mechanical hyperventilation and averaging of multiple ECG cycles. In 15 normal subjects, we show that hypocapnia (20 +/- 1 mmHg) significantly reduced mean T wave amplitude by 0.1 +/- 0.0 mV. Hypocapnia also increased mean heart rate by 4 beats/min without significantly altering blood pressure, ionized calcium or potassium levels, or the R wave or other features of the ECG. We therefore provide the first unequivocal demonstration that hypocapnia does consistently reduce T wave amplitude in normal, healthy subjects.
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PMID:Hypocapnia reduces the T wave of the electrocardiogram in normal human subjects. 1576 Nov 87

Cardiac toxicity is an uncommon side-effect of 5-fluorouracil (5-FU) treatment, consisting mainly of chest pain episodes with or without electrocardiographic changes and dysrhythmias. Here, we describe the case of a 56-year-old male patient with a diagnosis of advanced colorectal cancer who developed an acute myocardial infarction during 5-FU infusion. The patient was not affected by prior heart disease and did not show any classic risk factors for coronary heart disease. Coronary angiography examination revealed no evidence of coronary stenosis, supporting the hypothesis of a coronary artery spasm related to 5-FU infusion. Given the great number of cancer patients receiving 5-FU containing chemotherapeutic regimens, this rare but severe cardiac side-effect may be observed in both cardiologic and oncologic clinical practice. We suggest a tight clinical monitoring of all patients receiving 5-FU infusions, even in those without a prior history of heart disease.
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PMID:A case of acute myocardial infarction during 5-fluorouracil infusion. 1706 Aug 12

The causal associations between cigarette smoking and human diseases are irrefutable. In this review, we focus on the epidemiological pattern of cigarette smoking on cardiovascular risk, the underlying mechanistic process of such a causal link, how to prevent premature cardiovascular morbidity and mortality particularly through smoking cessation, and the health benefits of such cessation measures. Finally, we conclude our review summarizing a few of the proven evidence-based tobacco control strategies and policies from across the globe. We did not conduct a systematic review but followed a similar structure. We abstracted the most relevant published literature on the electronic databases, namely, PubMed, Embase and the Cochrane Library applying specific search terms. We also searched gray literature and consulted experts in the field for cross-references. Smoking has been estimated to cause about 11% of all deaths due to cardiovascular disease. Smoking contributes to the pathogenesis of coronary artery disease and sudden death through a variety of mechanisms, including the promotion of atherosclerosis, the triggering of coronary thrombosis, coronary artery spasm, and cardiac arrhythmias, and through reduced capacity of the blood to deliver oxygen. Smoking cessation also confers substantial benefits on people with serious heart disease. Smoking cessation should be viewed as therapeutic rather than preventive intervention, similar to treating asymptomatic hypertension. Smoking cessation is highly cost-effective relative to other frequently used medical and surgical interventions. Tobacco related illnesses are important public health issues worldwide. It has been estimated that there are 1.1 billion smokers worldwide and 250 million of them live in India.
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PMID:Smoking and cardiovascular health: a review of the epidemiology, pathogenesis, prevention and control of tobacco. 2007 56

Objective Life-threatening ventricular arrhythmias are recognized in patients with coronary spastic angina. Implantable cardioverter-defibrillators (ICDs) are effective in patients with structural heart disease and ventricular fibrillation. However, the optimal medication for patients with aborted sudden cardiac death (SCD) due to coronary artery spasm after the implantation of ICD remains controversial. Methods We investigated the medications and the numbers of appropriate ICD shocks in 137 patients with a history of aborted SCD due to coronary spasm. Results Appropriate ICD shocks were observed in 24.1% (33/137) of patients with aborted SCD due to coronary spasm during 41 months of follow-up. Only 15 (15.6%) of the 96 patients with ICDs received aggressive medical therapy, including two or three calcium-channel antagonists. The rate of appropriate ICD shocks was significantly higher in Western countries than in Asian countries (42.9% vs. 19.3%, p<0.01), whereas the medications did not differ between the two regions. Appropriate ICD shocks successfully resuscitated 33 patients. Three patients died due to second serious fatal arrhythmias. Conclusion Appropriate ICD shocks were recognized in a quarter of patients with aborted SCD due to coronary spasm and ICD implantation was effective for suppressing the next serious fatal arrhythmia in these patients. We should reconsider prescribing more medications after ICD implantation in patients with aborted SCD due to coronary artery spasm.
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PMID:Optimal Medications and Appropriate Implantable Cardioverter-defibrillator Shocks in Aborted Sudden Cardiac Death Due to Coronary Spasm. 2932 18


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