Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary arterial vasoconstriction, well recognized in Prinzmetal's variant angina, may participate in the pathogenesis of classic angina as well. Several recent studies in patients with obstructive coronary artery disease suggest that apparently spontaneous reductions in coronary blood flow can result in myocardial ischemia and even infarction. Evidence supporting the alpha adrenergic nervous system as a cause of such coronary vasoconstriction is reviewed, particularly the results of provocative testing with the cold pressor stimulus. Upon exposure of the skin to cold, patients with coronary artery disease demonstrate an inappropriate coronary vasoconstrictor response, often sufficient to produce angina. Normal patients, by contrast, show no change in coronary vascular resistance. In patients with a diseases coronary circulation, inappropriate vasoconstriction further restricts myocardial perfusion and appears to be little affected by beta adrenergic blocking agents or nitrates in the usual dosages. Nifedipine has proved effective in preventing coronary arterial spasm in patients with Prinzmetal's angina. Studies currently in progress suggest that it is also effective in blocking inappropriate coronary vasoconstriction in patients with typical angina. Nifedipine may thus be a useful addition to the treatment of ischemic heart disease.
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PMID:Inappropriate coronary vasoconstriction in patients with coronary artery disease: a role for nifedipine? 38 63

Vasospasms in the eye are often combined with digital vasospasms, as can be diagnosed with a nailfold capillaroscopic local cooling test. In 16 patients with a history of cold hands and feet the presence of peripheral vasospasms without any underlying disease was demonstrated by means of nailfold video-capillaroscopy. These patients showed the phenomenologic diagnosis of low-tension glaucoma with visual field defects characteristic of glaucoma even though intraocular pressure above 21 mmHg was excluded. The visual field defects were not homonymous, indicating a prechiasmal location of the vascular disturbance. Ocular vasospasms cause visual field damage that can be aggravated or provoked by cooling one hand in cold water and that often improves after treatment with the calcium channel blocker nifedipine. The results suggest that vasospasms not only are present in Raynaud's disease, migraine, and Prinzmetal's variant angina but also may be an important factor in the genesis of low-tension glaucoma. This is a new finding and may be related to a general vasospastic syndrome.
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PMID:Do vasospasms provoke ocular diseases? 231 50

Experimental data in animals indicate that coronary vasoconstriction occurs following blockade of the beta-adrenergic receptors or alpha-receptors activation. The vasomotor effects of these maneuvers in man are unclear. Therefore we investigated whether and to which extent alpha-stimulation (cold pressor test: CPT) and beta-blockade (propranolol) cause coronary vasoconstriction; whether this effect involves the resistance arterioles as well as the large epicardial branches, and, within these, whether the normal and stenotic tracts are involved. Patterns in patients with effort angina were compared with those in patients with Prinzmetal angina. We studied 19 cases with classic and 15 cases with Prinzmetal angina. The systemic, pulmonary and coronary hemodynamics (pressure, flow and resistance) and the vasomotor pattern of normal and stenotic epicardial branches (quantitative angiography) were evaluated in the baseline condition, during CPT, after propranolol (5 mg iv) and during CPT repeated after propranolol. We observed that: changes of the coronary flow due to beta-blockade and to CPT are related to the variations of the myocardial oxygen consumption, induced by the inhibition and activation of adrenergic receptors and not to the concomitant vasomotor reaction of the stenotic vascular tract; beta-blockade does not affect homogeneously the lumen of the stenotic lesions in effort angina and invariably increases the lumen in the Prinzmetal form; influences of CPT, in the absence as well as in the presence of beta-receptor blockade, on the lumen diameter of both normal vessels and stenotic lesions are minimal in either form of angina.
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PMID:[Activation and inhibition of adrenergic effects on the coronary vessels of patients with different forms of angina pectoris]. 255

The vasospastic diseases form an important group of ailments. The recognition of the different types of vasospasms is essential if the physician is to correctly advise and treat. Attention must be paid to the history of attacks of cold hands and feet combined with a predisposition to migraine and hypotension. The high prevalence of migraine, Raynaud's phenomenon. Prinzmetal's variant angina and visual acuity disturbance of ophthalmologically unexplained origin in patients with peripheral vasospasms indicates the existence of a generalized vasospastic disease. There is most often no underlying disease detectable. In cases of unknown origin, supplementary investigations are necessary. The management of vasospastic disorders is still unsatisfactory at the present time. These difficulties reflect the uncertainty in the etiology and pathogenesis of the disorder.
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PMID:[Raynaud's syndrome: diagnosis and therapy in general practice]. 267 63

A local cooling test produces a typical flow stop reaction in nailfold capillaries in 88% of patients with Raynaud's phenomenon, but only in 15% of healthy controls. A stop reaction occurred in 9 of 12 patients with Prinzmetal variant angina, exceeding significantly that in 2 of 12 matched control subjects. Also in patients with reversible visual disorders presumably due to vasospasm, the test resulted in a stop reaction in 16 of 25 cases exceeding that in control. In both of these patient groups the cooling test as well as the symptoms reacted favorably to nifedipine. Thus, the local cold exposure test appears to be useful for objective clinical examination not only of patients with Raynaud's phenomenon but also of patients with vasospastic syndromes such as variant angina and visual disorders.
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PMID:Local cooling test for clinical capillaroscopy in Raynaud's phenomenon, unstable angina, and vasospastic visual disorders. 280 Jun 80

Peripheral vascular resistance (PVR) and thromboxane A2(TxA2) synthesis after the cold pressor test were investigated in different subsets of patients with angina (10 with stable effort angina, 36 with resting angina [24 in an active phase and 12 in an inactive phase], and five with Prinzmetal's variant angina) and in 41 control subjects of equivalent age and risk factors. Left ventricular end-diastolic pressure, ejection fraction, extent of coronary angiographic lesions, and baseline PVR were not significantly different among the various patient groups. In all patient groups, except those with variant angina, the cold pressor test resulted in a higher increase in PVR than in the control subjects (p less than .001 for all groups). In patients with variant angina the vasoconstrictor response was increased only in proximity (about 1 hr) to ischemic attacks. In patients with active resting angina the vasoconstrictor response was on the average four times longer than that in patients with effort angina and with inactive resting angina (p less than .001). This exaggerated vasoconstrictor response was associated with elevated TxA2 resting levels in plasma and with increased TxA2 synthesis after the cold pressor test. A linear relationship was found between the area of the vascular response and the area of TxA2 production after the cold pressor test in patients with active resting angina (r = .87, p less than .001). The increased TxA2 synthesis and the inappropriate increase of peripheral vascular response to sympathetic stimulation revert back to normal in the inactive phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced peripheral vasoconstrictor response and increased thromboxane A2 synthesis after the cold pressor test in patients with angina at rest. 394 51

The presentation, diagnosis (including provocative testing), and therapy of Prinzmetal's variant angina are reviewed. Prinzmetal's variant angina (PVA) is a form of angina caused by coronary-artery vasospasm (CAS) and is not associated with exertion. It is diagnosed by history, electrocardiogram, or coronary-artery angiography. Provocative tests, such as the cold-pressor test or intravenous ergonovine maleate, are sometimes used to aid diagnosis of PVA. Nitrates, adrenergic - blocking agents, and calcium-channel blocking agents can be used in treating PVA. Nitroglycerin and isosorbide dinitrate effectively relieve CAS. However, long-term prospective studies on the use of these drugs for PVA are lacking in the literature. Studies on treating PVA with adrenergic-blocking agents have been equivocol, with some studies reporting improvement and some reporting worsening. Calcium-channel blocking agents are promising drugs for PVA. Nifedipine is generally considered the prototype of this class for antianginal activity. It is administered orally in PVA patients and is effective. Side effects are mild and do not usually require termination of therapy. Verapamil hydrochloride, the prototype calcium-channel blocking agent for arrhythmias, is effective for PVA, but only 10-20% of an orally administered dose reaches systemic circulation because of the first-pass effect. Other calcium-channel blockers, including perhexilene maleate, diltiazem hydrochloride, prenylamine, and lidoflazine, have been tested in a few CAS patients with some success; adverse effects and toxicities limit the use of some of them, especially perhexilene. Therapy, using combinations of nitrates, adrenergic-blocking agents, and calcium-channel blocking agents, is needed in some patients. Dosing guidelines for all drugs are given in the paper. Treatment of PVA should begin with oral nitrates. Calcium-channel blocking agents are indicated in the patient who has failed to respond or is intolerant to maximum doses of nitrates given in various forms.
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PMID:Diagnosis and treatment of Prinzmetal's variant angina. 676 60