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

Factors involved in the development of coronary atherosclerosis and the possible role of estrogens in its development are discussed. Risk factors in the development of atherosclerosis include hyperlipemia, hypertension, cigarette smoking, and diabetes. However, the incidence of heart disease and presence of risk factors are also related to heredity, geography, and socioeconomic conditions, and to diet, exercise, and emotional stress. Contrary to previous belief, high doses of estrogens aggravate the condition of men and menopausal women at risk of heart attack. Although estrogens do not markedly alter cholesterol levels, they do tend to elevate triglyceride levels and contribute to hyperlipemia. They are also associated with diabotegenic sequelae and hypertension. Pregnancy and estrogens increase blood clotting Factors VII and X, accelerate prothrombin time, shorten clotting time, and incre ase platelef aggregation. Further research into the role of estrogens in the development of atherosclerosis is recommended.
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PMID:Estrogens and atherosclerosis. 99 76

It is often difficult to assess cases in which the circumstances strongly indicate traumatic cause of death, while the autopsy reveals no life-threatening injuries. Such cases can be divided into three groups: 1) death explained by heart disease and emotional stress and/or physical exertion; 2) deaths by suspected traumatic vagal inhibition in which another cause of death is found or the cause of death remains obscure, sometimes depending on incomplete postmortem investigation; and 3) death established by autopsy, but difficult to ascertain if there is a connection between the cause of death and the trauma.
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PMID:Questionable traumatic deaths and their assessment. 685 5

Myasthenia gravis (MG) is an antibody-mediated muscle disease in which any skeletal muscle can be affected. MG may produce numerous symptoms and signs. To doctors and patients, it may seem like lung disease, stroke, heart disease, or the effects of emotional stress. This article explores the "territory" between MG and diseases of the heart and lungs as well as the other neuromuscular diseases.
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PMID:Clinical features of myasthenia gravis. 804 40

The reports relating emotional stress to sudden death are largely anecdotal. In addition to experimental and electrophysiological studies, an opportunity for a better understanding of possible stress-related sudden death (SSD) may be provided by medicolegal autopsies. The goal of our autopsy study was to analyze cardiovascular pathologic findings in cases of SSD and if possible identify mechanisms by which the stressful event (SE) could be the cause. Forty three cases were studied (29 males and 14 females). In all cases, the SE and the death were witnessed. The age range was 22 to 90 years in males (mean, 52) and 30 to 92 years in females (mean, 64). Death occurred in all cases without premonitory symptoms. In 20 cases, death occurred during the SE and in the other 23 cases occurred within 2 h of the event. SE included fear, 15 cases; altercation, 21 cases; sexual activity, 3 cases; police questioning or arrest, 4 cases. According to police reports, in 40 cases (90%), the victims had no previous clinical history of cardiovascular disease. At autopsy, the heart weight in males ranged from 255 to 1000 g with a mean of 517 g and in females the range was 250-700 g with a mean of 417 g. In only 3 cases, gross and microscopic examination of the heart was normal. In 2 of the remaining 40 cases the subjects died of subarachnoid hemorrhage. In 38 cases, a cardiac cause of death was found as follows: coronary heart disease, 27 cases; cardiomyopathy, 6 cases; aortic valvular stenosis, 2 cases and right ventricular dysplasia, 3 cases. A coronary artery thrombosis was found in 8 cases of sudden coronary death. Post myocardial infarction fibrosis was present in 25 cases (92%) of sudden coronary death. In conclusion, it appears from our autopsy study that SSD occurs primarily in those individuals with severe heart disease, especially coronary heart disease.
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PMID:Stressful events as a trigger of sudden death: a study of 43 medico-legal autopsy cases. 906 8

We report a 13-year-old girl with extensive striae and an acneiform eruption following surgery for complex congenital heart disease. These findings were associated with elevated serum and urinary cortisol levels with loss of diurnal rhythm. The resolution of the eruption and the fading of her striae coincided in time with normalization of her blood parameters on day 72 postoperatively. We conclude that the cause of steroid excess in our patient was stress induced by the cardiac surgery and a complicated and protracted postoperative course. To our knowledge, this is the first report in the English language literature of skin changes due to endogenous hypercortisolaemia caused by intense physical and emotional stress.
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PMID:Striae and acne following cardiac surgery in a child. 1023 32

Research has developed a concrete link between psychological/emotional stress and life-threatening diseases such as heart disease and cancer. Here we present a technique to assess the magnitude of stress from cholesterol variation number (CVN). This number is the difference between the highest and the lowest cholesterol concentrations that relates to the five hourly cholesterol measurements performed over a five hour span. Since cholesterol in serum arises from the liver, the CVN is equated with the fluctuations in hepatic biosynthesis. This relationship is explained on the basis of the rhythmic hormonal secretions associated with cholesterol biosynthesis. Whenever stress-induced aberrations in timing of hormonal secretions occur, CVN changes. Individuals with lower CVN would have overall better health than persons with higher CVN. Thus by utilizing CVN, physicians may be able to differentiate cardiovascular health of individuals with the same or very similar serum cholesterol concentrations.
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PMID:Five hourly measurements of serum cholesterol levels: a new methodology to assess and evaluate stress, good health and disease. 1086 48

Catecholamine-induced polymorphic ventricular tachycardia (CPVT), a rare disease that occurs in subjects without obvious organic heart disease, is characterized by episodes of syncope, seizures, or sudden death in response to physiologic or emotional stress. This report reviews evidence that a missense mutation in the CASQ2 gene is associated with autosomal-recessive CPVT.
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PMID:A missense mutation in the CASQ2 gene is associated with autosomal-recessive catecholamine-induced polymorphic ventricular tachycardia. 1273 48

The sudden death of a person caused by an arrhythmia that is induced by physical and/or emotional stress provoked by the criminal activity of another person is sometimes referred to as "homicide by heart attack." Published criteria for such an event relate to situations where no physical contact occurs between the perpetrator and the victim. Situations involving physical contact, but with absence of lethal injuries, are frequently treated is a similar fashion by forensic pathologists. Herein, we propose a set of modified criteria, which include cases where physical contact has occurred. Five examples of so-called "homicide by heart attack" are presented, including a 40-year-old man who was struck in the head with a wooden statue, a 74-year-old man who was punched in the jaw by a robber, a 66-year-old woman who was started awake by a home-intruder, a 67-year-old woman who struggled with a would-be purse-snatcher in a parking lot, and a 52-year-old man who was in a physical altercation with a younger man. In each instance, autopsy revealed the presence of severe, underlying heart disease, as well as absence of lethal injuries. In each case, investigative information was such that the emotional and/or physical stress associated with the criminal activity of another individual was deemed contributory to the death. The presumed mechanism of death in each case was a cardiac dysrhythmia related to underlying heart disease, but initiated by the emotional and/or physical stress.
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PMID:"Homicide by heart attack" revisited. 1517 Nov 83

Patients with cardiac disease typically develop life-threatening ventricular arrhythmias during physical or emotional stress, suggesting a link between adrenergic stimulation and regulation of the cardiac action potential. Human ether-a-go-go related gene (hERG) potassium channels conduct the rapid component of the repolarizing delayed rectifier potassium current, I(Kr). Previous studies have revealed that hERG channel activation is modulated by activation of the beta-adrenergic system. In contrast, the influence of the alpha-adrenergic signal transduction cascade on hERG currents is less well understood. The present study examined the regulation of hERG currents by alpha(1A)-adrenoceptors. hERG channels and human alpha(1A)-adrenoceptors were heterologously coexpressed in Xenopus laevis oocytes, and currents were measured using the two-microelectrode voltage clamp technique. Stimulation of alpha(1A)-receptors by applying 20 microM phenylephrine caused hERG current reduction due to a 9.6-mV shift of the activation curve towards more positive potentials. Simultaneous application of the alpha(1)-adrenoceptor antagonist prazosin (20 microM) prevented the activation shift. Inhibition of PKC (3 microM Ro-32-0432) or PKA (2.5 microM KT 5720) abolished the alpha-adrenergic activation shift, suggesting that PKC and PKA are required within the regulatory mechanism. The effect was still present when the PKA- and PKC-dependent phosphorylation sites in hERG were deleted by mutagenesis. In summary, cardiac repolarizing hERG/I(Kr) potassium currents are modulated by alpha(1A)-adrenoceptors via PKC and PKA independently of direct channel phosphorylation. This novel regulatory pathway of alpha1-adrenergic hERG current regulation provides a link between stress and ventricular arrhythmias, in particular in patients with heart disease.
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PMID:Activation of cardiac human ether-a-go-go related gene potassium currents is regulated by alpha(1A)-adrenoceptors. 1536 37

Cardiovascular reactivity, an abrupt increase in blood pressure and heart rate in response to emotional stress, is a risk factor for hypertension and heart disease. Brain angiotensin II (Ang II) type 1 (AT(1)) receptor is increasingly recognized as an important regulator of cardiovascular reactivity. Given that a wide variety of AT(1) receptor signalling pathways exists in neurones, the precise molecular mechanisms that underlie central cardiovascular actions of Ang II during emotional stress are yet to be determined. Growing evidence, however, indicates that reactive oxygen species, and in particular superoxide (.O(2)(-)), are important intracellular messengers of many actions of brain Ang II. In particular, studies employing microinjection of .O(2)(-) scavengers directly into the rostral ventrolateral medulla (RVLM) and dorsomedial hypothalamus of rabbits have shown that the activation of AT(1) receptor-.O(2)(-) signalling is required for full manifestation of the cardiovascular response to emotional stress. This role of .O(2)(-) appears to be highly specific, because .O(2)(-) scavengers in the RVLM do not alter the sympathoexcitatory response to baroreceptor unloading or sciatic nerve stimulation. The subcellular mechanisms for the stress-induced .O(2)(-) production are likely to include the activation of NADPH oxidase and are essentially independent of nitric oxide. This review summarizes current knowledge of redox-sensitive signalling mechanisms in the brain that regulate cardiovascular effects of stress. Additionally, it presents initial evidence that .O(2)(-) may be less important in the activation of central pressor pathways mediating cardiovascular arousal associated with appetitive events, such as food anticipation and feeding.
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PMID:Brain superoxide as a key regulator of the cardiovascular response to emotional stress in rabbits. 1730 48


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