Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

The heart rate response to standing, cough, hand grip, and deep breathing were examined in normal subjects and coronary artery disease patients (greater than 70% diameter narrowing). The heart rate responses to these maneuvers were reduced in coronary patients and in anginal patients with normal coronary angiograms, as compared to normals. Detection (with the heart rate response to standing) was determined by using an RR interval cutoff of 140 ms for males and 120 ms for females discriminated between normals and CAD patients. In men sensitivity was 0.58, specificity 0.87 and CCR 0.75, and in women sensitivity was 0.67, specificity 0.79 and CCR 0.75. These values are similar to those reported for ST segment depression in similar populations. When separating normals from those with 2 and 3 vessel disease--sensitivity is 0.67, specificity 0.87, predictive value 0.71 and CCR 0.80. The response to cough, hand grip, and deep breathing showed similar trends but had less specificity than the response to standing. Thus, the heart rate response to most autonomic maneuvers is blunted in subjects with coronary disease and in those with pain syndromes sent for coronary angiography. These findings need testing in larger populations but autonomic maneuvers fail to discriminate patients with coronary disease from those with normal angiograms presenting with chest pain syndromes.
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PMID:Autonomic responses in chest pain syndromes as compared to normal subjects. 381 52

This article is a review of the use of prophylactic lidocaine as a preintubation medication. Intubation is associated with a cardiovascular response of elevated blood pressure and pulse, cough reflexes, occasional dysrhythmias, increased intracranial pressure, and increased intraocular pressure. In patients with atherosclerotic heart disease, potential intracranial lesions, and potential penetrating eye injuries, these responses to intubation are of greater risk. Various studies have reviewed the effect of lidocaine to blunt these responses. It is agreed that lidocaine blunts cough reflexes and dysrhythmias. Some studies note a response of lidocaine in blunting rises in pulse, blood pressure, intracranial and intraocular pressure. No studies document any harmful effects of prophylactic lidocaine given preintubation. A dose of prophylactic lidocaine of 1.5 mg/kg given intravenously 3 minutes before intubation is optimal. For suctioning of intubated patients, lidocaine can be given endotracheally in a 5-6 mg/kg dose diluted in 6 cc via simple administration at the entrance to the endotracheal tube.
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PMID:Prophylactic lidocaine use preintubation: a review. 796 97

The common symptoms of constrictive pericarditis, i.e. dyspnea on exertion, shortness of breath and cough, relate to impairment of ventricular filling and to a progressive rise in systemic and pulmonary venous pressures. Myocardial ischemia, angina and myocardial infarction are rarely associated with this disease. We have encountered two patients with constrictive pericarditis, one presenting with angina and the other with acute anterior wall infarction. Possible etiologies of constrictive pericarditis in the first case include cardiac surgery, chronic renal failure and myocarditis; in the second case, Crohn's disease. The proposed mechanism of chest pain in the first patient was a reduced cardiac output resulting in underperfusion of the coronary arteries, although it is possible that the patient experienced angina due to the presence of severe coronary artery disease. In the second patient an anterior wall infarction and post-infarction angina were attributed to obliteration of the left anterior descending artery by constraint of a thickened pericardium. In both cases non-invasive imaging modalities were not of use in establishing the diagnosis of constrictive pericarditis. Clinical awareness and accurate hemodynamic measurements continue to play a key role in the diagnostic process.
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PMID:Observations of angina and myocardial infarction in constrictive pericarditis. 831 45

The clinical course of congestive heart failure (CHF) and mitral valve stenosis (MVS) is accompanied by episodes of dyspnea, wheezing, and cough, symptoms also observed in patients with bronchial hyperreactivity. However, it is still controversial whether bronchial hyperreactivity is demonstrable in patients with chronic overload of the pulmonary circulation. In order to examine the effects of CHF on the respiratory function, we performed pulmonary function tests, titrated bronchial acetylcholine provocations, and left and right heart catheterization in 21 patients with impaired left ventricular function (mean ejection fraction, 37 percent, NYHA class 3), 5 patients with MVS, and 17 control patients with coronary artery disease (mean ejection fraction, 63 percent). Bronchial hyperresponsiveness was defined as an obstructive response to increased doses of inhaled acetylcholine. A 20 percent fall in forced expiratory volume in the first second (FEV1), a 100 percent increase in total airway resistance (Rtot), and a 60 percent reduction of pulmonary conductance (SGtot) were considered positive. Patients with impaired left ventricular function showed significantly higher airway resistance, and lower airway conductance at the maximal tolerated acetylcholine dose compared with control patients. Patients with MVS had a significant lower airway conductance. The induced bronchial obstruction was completely reversible upon inhalation of a beta 2-mimetic. We conclude that chronic overload of the pulmonary circulation is accompanied by bronchial hyperreactivity that may augment the symptoms of dyspnea in patients with CHF and MVS.
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PMID:Bronchial hyperreactivity in patients with moderate pulmonary circulation overload. 848 30

As a net effect of ACE-inhibitors and AT1-receptor antagonists on the renin-angiotensin system (RAS) cardioprotection due to vasodilative (reduction of blood pressure, afterload reduction), antiproliferative (reduced cell growth, reduction of "vascular" and/or "ventricular remodeling", reduced formation of extracellular matrix), as well as antiadrenergic actions and due to the stimulating effect on natriuresis, reduction of blood pressure, preload reduction can be expected. These aims of therapy have mostly been confirmed for the action of ACE-inhibitors by experimental and clinical studies but except for the treatment of arterial hypertension and few preliminary reports concerning the treatment of cardiac dysfunction, no comparable data are available for AT1-receptor antagonists. To date, an antithrombotic and profibrinolytic action could only be demonstrated for ACE-inhibitors. This effect has been discussed to be responsible for the improvement of long-term prognosis in patients with coronary artery disease. Despite the similar spectrum of action there exist important differences between ACE-inhibitors and AT1-receptor antagonists that might underline the need of an individual use of these drugs: the dual action of ACE-inhibitors on the RAS and the kinin system bears many benefits but has been also shown to be accompanied by side-effects, mainly chronic dry cough, in a relatively high percentage of patients thus leading to discontinuation of therapy in 8-14%. This respective side-effect can be prevented by the use of AT1-receptor antagonists. It has been discussed whether the incomplete action of ACE-inhibitors on AT1-receptor-mediated effects is at least in part responsible for the efficacy of this drug which is relatively high (75-80%) as compared to other substances. Due to their direct action, AT1-receptor-blockers might also be of high effectiveness for the treatment of severe heart failure. A combination of the ACE-inhibitor-mediated activation of the kinin-system with the more specific blockade of AT1-receptors by AT1-receptor antagonists might be of benefit and is currently under investigation. Finally, it has been discussed that the increased AT II concentration in case of AT1-receptor-blockade activates AT2-receptor-mediated mechanisms thus leading to an additive vasoprotective effect.
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PMID:[Pathophysiological mechanisms of the renin-angiotensin system and its pharmacologic modification by ACE inhibitors or angiotensin II (type 1) receptor blockers in cardiovascular diseases]. 923 95

The pharmacology, pharmacokinetics, clinical uses, adverse effects, drug interactions, dosage, cost, and therapeutic interchange of oral angiotension-converting-enzyme (ACE) inhibitors are reviewed. ACE inhibitors attenuate the formation of angiotension II and may lead to the accumulation of kinins. Although the hypotensive effects of many ACE inhibitors may persist for 24 hours, some patients require more than one dose per day to achieve adequate control. These agents accumulate in patients with renal or hepatic dysfunction, but it is unclear whether dosage adjustments are necessary. ACE inhibitors are effective against mild to moderate hypertension; for severe hypertension, additional anti-hypertensive agents may be necessary. Other conditions in which ACE inhibitors have shown efficacy include congestive heart failure, myocardial infarction, left ventricular dysfunction, left ventricular hypertrophy, chronic renal insufficiency, insulin sensitivity, and coronary artery disease. The most common adverse effect is a persistent nonproductive cough. Angioedema, fetal and neonatal morbidity and mortality, acute renal failure, and hyperkalemia may also occur. ACE inhibitors may interact with diuretics, lithium, nonsteroidal anti-inflammatory drugs, oral hypoglycemic agents, and some other drugs. ACE inhibitor therapy should be initiated with low doses that may then be slowly adjusted upward. Many of the agents have similar costs for lower and higher dosages. The only significant differences among the ACE inhibitors are the time of onset of hypotensive effects, time to peak effect, and duration of effect. Each formulary should include, at least, captopril and one intermediate-acting and one long-acting ACE inhibitor.
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PMID:Oral angiotensin-converting-enzyme inhibitors. 940 13

Headaches that have an explosive onset with exercise, including sexual activity, generally are benign in origin. A subarachnoid hemorrhage, a mass lesion in the brain, or an anomaly of the posterior fossa must be considered, however. The mechanisms that produce sexually induced or cough headaches of abrupt onset are unknown. It is known, however, that a rapid increase in intrathoracic pressure suddenly reduces right atrial pressure and presumably decreases venous sinus drainage from the brain. This situation results in a transient increase in intracranial pressure. Jaw pain that occurs with chewing often is considered to be TMJ dysfunction when arthritic in quality and if subluxations of the jaw can be shown on the physical examination. Giant cell arteritis and common or external carotid artery occlusive disease should be considered when the pain is ischemic in quality. An anginal equivalent is another possibility. Headaches that worsen with vigorous exercise are commonly migrainous. When their onset is apoplectic with exertion (particularly exertion against a closed glottis), the most likely diagnoses are increased intracranial pressure, a posterior fossa abnormality, or benign exertional headaches. Most cardiac induced headaches, but not all, are of a more gradual onset. If there are significant risk factors for coronary artery disease, an exercise stress test is appropriate. A therapeutic trial of nitroglycerin may help to establish a diagnosis if it improves the headache. Using antimigraine drugs as a diagnostic test is inappropriate because triptans and ergots are contraindicated in the presence of coronary artery disease, and a positive response is not diagnostic of migraine.
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PMID:A spectrum of exertional headaches. 1148 Feb 60

Previous studies showed that increased QT dispersion (QTd) has been observed during episodes of myocardial ischemia or infarction and identify the patients at risk of arrhythmia or sudden death. The objective of this study is to investigate the relationship between coronary artery disease and QTd during the Valsalva maneuver. The study population included 85 subjects (21 with normal coronary arteries, 35 with stable angina pectoris, and 29 with unstable angina pectoris). Twelve-lead surface ECGs were recorded at 50-mm/sec paper speeds and were obtained before the Valsalva maneuver and during the strain phase. The results indicate a significant difference in mean time increase between the control group and the group with stable angina pectoris (mean difference = 16.10 milliseconds, p<0.000), and between the control group and the group with unstable angina pectoris (mean difference = 35.26 milliseconds, p<0.000). The mean difference in time between these groups was also compared (mean difference = 19.17 milliseconds), and was statistically significant (p<0.000). There are some conditions like constipation, severe coughing spells, nausea, vomiting, and carrying or lifting heavy objects that increase intrathoracic pressure and may increase QT dispersion. Therefore, all these conditions should be treated appropriately and carrying or lifting heavy objects is forbidden, especially in patients with coronary artery disease.
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PMID:Effects of Valsalva maneuver on QT dispersion in patients with ischemic heart diseases. 1171 25

Angiotensin-converting enzyme (ACE) inhibitors and more recently angiotensin-receptor blockers (ARBs) have become popular therapies in the end-stage renal disease (ESRD) patient. The ability of either of these drug classes to reduce blood pressure in the ESRD patient is well accepted; however, there is considerably less information available to guide the clinician in the safe and effective use of these drugs in the ESRD patient with congestive heart failure and/or coronary artery disease. Head-to-head studies in the ESRD patient are lacking for both drug classes. Several pharmacokinetic factors can influence the selection of these drugs, including dialysability and the propensity for systemic accumulation. ACE inhibitors (ACE-Is) and ARBs are recognised as having a range of nonpressor effects that are pertinent to patients with ESRD. Such effects include their ability to decrease both thirst drive and erythropoiesis. These drug classes, though, are distinguishable by the unique adverse effect profile for ACE-Is. As is the case in patients without renal failure, ESRD patients can experience cough and, less frequently, angioneurotic oedema with ACE-Is. In the ESRD population, so-called anaphylactoid dialyser reactions can occur in conjunction with ACE-I use. The use of a drug from within the ARB class carries both less risk and permits a compound with a preferred pharmacokinetic profile limited dialysability and minimal systemic accumulation to be administered. These attributes would favour the increased use of ARBs in this population.
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PMID:The pharmacokinetics and pharmacodynamics of angiotensin-receptor blockers in end-stage renal disease. 1258 68


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