Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with panic disorder often complain of angina-like chest pain during panic attacks, but this is not usually considered life-threatening. We describe three patients with panic disorder and documented cardiac ischaemia during episodes of chest pain. In two, it progressed to myocardial infarction. As none had atherosclerosis evident at coronary angiography, the mechanism was presumed to be coronary artery spasm. These cases illustrate that pain typical of angina during panic attacks may have an organic cause.
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PMID:Panic disorder: coronary spasm as a basis for cardiac risk? 959 45

Regional sympathetic activity can be studied in humans using electrophysiological methods measuring sympathetic nerve firing rates and neurochemical techniques providing quantification of noradrenaline spillover to plasma from sympathetic nerves in individual organs. Essential hypertension: Such measurements in patients with essential hypertension disclose activation of the sympathetic outflows to skeletal muscle blood vessels, the heart and kidneys, particularly in younger patients. This sympathetic activation, in addition to underpinning the blood pressure elevation, most likely also contributes to left ventricular hypertrophy, and to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidaemia. Antihypertensive drugs, such as moxonidine, which act primarily by inhibiting the sympathetic nervous system, should have additional clinical benefits beyond those attributable to blood pressure reduction, in protecting against hypertensive complications. Obesity-related hypertension: Understanding the neural pathophysiology of hypertension in the obese has been difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac noradrenaline spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal noradrenaline spillover, but without suppression of cardiac sympathetics (cardiac sympathetic activity being more than double that of normotensive obese and 25% higher than in healthy volunteers). Increased renal sympathetic activity in obesity may be a 'necessary' cause for the development of hypertension (and predisposes to hypertension development), but apparently is not a 'sufficient' cause. The discriminating feature of the obese who develop hypertension is the absence of the adaptive suppression of cardiac sympathetic tone seen in the normotensive obese. Heart failure: In cardiac failure, the sympathetic nerves of the heart are preferentially stimulated. Noradrenaline release from the failing heart at rest in untreated patients is increased as much as 50-fold, similar to the level seen in the healthy heart during near-maximal exercise. Activation of the cardiac sympathetic outflow provides adrenergic support to the failing myocardium, but at a cost of arrhythmia development and progressive myocardial deterioration. Psychosomatic heart disease: No more than 50% of clinical coronary heart disease is explicable in terms of classical cardiac risk factors. There is gathering evidence that psychological abnormalities, particularly depressive illness, anxiety states, including panic disorder and mental stress, are involved here, 'triggering' clinical cardiovascular events, and possibly also contributing to atherosclerosis development. The mechanisms of increased cardiac risk attributable to mental stress and psychiatric illness are not entirely clear, but activation of the sympathetic nervous system seems to be of prime importance.
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PMID:Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease. 1134 14

The article reports a case of ischemic heart disease (IHD) diagnosed in a patient admitted to hospital because of recurrent paroxysms of panic disorder. Clinical follow-up determined some significant risk factors of IHD, the clinical picture of which was overlapped by dominating anxiophobic and tanatophobic syndrome. Diagnosis of IHD and coronary atherosclerosis was made at radionuclide single photon computed tomography of the myocardium, which had detected hypoperfusion of the posteroseptal left ventricle, followed by coronaroventriculography. This case illustrates the necessity of the integrative (psychosomatic) approach to diagnosis and choice of treatment policy.
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PMID:[Panic disorder in clinical picture of ischemic heart disease]. 1236 Jun 14

The association between panic disorder (PD) and cardiovascular diseases (CVD) has been extensively studied in recent years and, although some studies have shown anxiety disorders co-existing or increasing the risk of heart disease, no causal hypothesis has been well established. Thus, a critical review was performed of the studies that evaluated the association between PD and cardiovascular diseases; synthesizing the evidence on the mechanisms mediators that theoretically would be the responsible for the causal pathway between PD and CVD, specifically. This overview shows epidemiological studies, and discusses biological mechanisms that could link PD to CVD, such as pleiotropy, heart rate variability, unhealthy lifestyle, atherosclerosis, mental stress, and myocardial perfusion defects. This study tried to provide a comprehensive narrative synthesis of previously published information regarding PD and CVD and open new possibilities of clinical management and pathophysiological understanding. Some epidemiological studies have indicated that PD could be a risk factor for CVD, raising morbidity and mortality in PD, suggesting an association between them. These studies argue that PD pathophysiology could cause or potentiate CVD. However, there is no evidence in favour of a causal relationship between PD and CVD. Therefore, PD patients with suspicions of cardiovascular symptoms need redoubled attention.
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PMID:Panic disorder and cardiovascular diseases: an overview. 2889 14