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)

Cardiac hypertensive structural changes, catecholamine-related cardiomyopathy, and congestive heart failure (CHF) have been encountered in pheochromocytoma, as a result of prolonged exposure to high concentrations of endogenous catecholamines. A 34-year-old man presented with severe hypertension, cardiomegaly, and CHF, presumably as a result of continuous alpha-adrenergic intoxication with oxymetazoline hydrochloride, phenylephrine hydrochloride, and ephedrine hydrochloride, consumed in massive doses by an overuse of nasal decongestants and cough syrup (daily doses of 20, 100, and 300 mg, respectively). Coadministered chlorpromazine hydrochloride and trimeprazine tartrate may have also contributed to the clinical presentation through their anticholinergic and antihistaminic properties. The possibility of an overuse of these over-the-counter drugs should be considered in the differential diagnosis of hypertensive emergencies, especially with the simultaneous use of anticholinergic and antihistamine medications, beta-blocking agents, or monoamine oxidase inhibitors.
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PMID:Hypertensive crisis from chronic intoxication with nasal decongestant and cough medications. 172 79

It is known that patients suffering from severe cardiomyopathy may develop cyclic changes in breathing (Cheyne-Stokes-breathing) (2, 3). Coughing and dyspnea may be linked to periodic breathing. Specific detailed polysomnographic studies of sleep architecture and oxygen saturation have not been published. Eight patients suffering from dilatative cardiomyopathy (NYHA III-IV) were studied by pulse oximetry and polysomnography. Six of eight patients had severe breathing irregularities. These disturbances became manifest partially as Cheyne-Stokes breathing, partially as central sleep apnea. During these periods, oxygen saturation dropped as far as to 65 per cent of the original level.
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PMID:[Oxygen saturation and sleep structure in patients with dilated cardiomyopathy]. 186 3

Autopsy studies have shown that cardiomyopathy of Duchenne's muscular dystrophy (DMD) is characterized by fibrosis of the posterobasal and contiguous lateral wall of the left ventricle. This study was designed to determine whether stress testing would improve the sensitivity of echocardiography to detect secondary impairment of regional myocardial function. 12 patients aged 5 to 23 years with DMD were investigated. TM- and 2D-echocardiograms were performed before and during graded infusion of angiotensin (A) (0.5 to 5.0 mcg/min), and parameters of cardiac function analyzed. Satisfactory echocardiograms were obtained in all patients. Stress testing with A proved feasible in DMD and did not interfere with echocardiography. Before A all patients were in regular sinus rhythm and free of cardiac symptoms. Left ventricular function was normal in 9 patients and considered abnormal in 3 patients with hypokinesis and increased echo intensity of the posterobasal and lateral wall (2D short axis view) and/or a posterior wall to septal amplitude ratio of less than or equal to 1.1 (TM-echocardiogram). During A mean blood pressure rose and heart rate dropped significantly. 9 patients had marked supraventricular arrhythmias, 8 complained of dyspnea, cough or chest pain. Hypo- or akinesis of the posterobasal and sometimes the lateral wall was seen in 8, and a posterior wall to septal amplitude ratio of less than or equal to 1.1 in 9 patients. 3 patients, all with a muscle score of 60% or higher, remained free of symptoms and had no regional contraction abnormalities. Thus, clinical symptoms during A suggested latent congestive heart failure in many of the patients, and echocardiography identified provokable contraction abnormalities of such segments of the ventricular wall known to be most frequently involved in the dystrophic process in DMD. Stress testing revealed a correlation between clinical symptoms, abnormal echocardiographic findings and extent of the skeletal muscle disease in our study group. Physical limitation seems to protect the heart against demands that would otherwise cause earlier clinical manifestation of the cardiomyopathy in DMD.
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PMID:[Cardiac manifestation of progressive muscular dystrophy of the Duchenne type]. 378 61

Thirteen patients with Duchenne's muscular dystrophy underwent spinal fusion and Harrington instrumentation between 1967 and 1979. Curve progression was the most common indication for surgery. Cardiorespiratory evaluation was most important in the timing of surgery. After 12 months of immobilization, all spines fused. Major and minor complications occurred in eight of 13 patients. The major benefit of surgery was improved or maintained sitting balance. Surgery is not recommended for patients with symptomatic cardiomyopathy, vital capacity less than 40%, a nonfunctional cough, or rapidly progressive deterioration in muscle strength with a projected life span of less than two years.
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PMID:Spinal fusion in Duchenne's muscular dystrophy. 717 88

This paper investigates the role of carnitine in the etiology and treatment of dilated cardiomyopathy in boxers. Two boxers were diagnosed as having dilated cardiomyopathy on the basis of clinical presentation, chest radiographs, electrocardiography and echocardiography. In one dog, carnitine was administered at 6.0 g (or approximately 250 mg/kg live weight (LW) daily per os, and this dog remained asymptomatic for 4 mo until it presented for anorexia, coughing and weakness. Necropsy and histologic findings were consistent with boxer cardiomyopathy in both dogs. Cardiac carnitine concentration was 567 nmol/g wet weight in the unsupplemented dog, which is below the normal mean +/- SD concentration of 1493 +/- 141 nmol/g wet weight. Low cardiac carnitine concentrations appear to be a consistent finding for dilated cardiomyopathy in boxers. However, in the dog that received carnitine therapy, cardiac carnitine was 2802 nmol/g wet weight, and all tissues assayed in the supplemented dog had higher carnitine concentrations than normal dogs. Elevation of tissue carnitine failed to ameliorate dilated cardiomyopathy in this dog. Oral carnitine supplementation in these therapeutic doses appears not to resolve dilated cardiomyopathy in all boxers.
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PMID:Case report: efficacy of oral carnitine therapy for dilated cardiomyopathy in boxer dogs. 799 70

Lidocaine-induced seizures have been reported after topical administration. A 30-year-old, 48-kg women with acquired immunodeficiency syndrome, chronic end-stage renal failure, anemia, congestive heart failure (CHF), cardiomyopathy, and increased liver function tests was admitted to the hospital with fever, chills, and dry cough. Bronchoscopy was performed to rule out Pneumocystis carinii pneumonitis; the patient experienced seizure activity after administration of a total dose of topical lidocaine 300 mg. Plasma drug concentration measured shortly after seizure, and at 4 and 22 hours after seizure were 12.0, 7.6, and 1.4 mg/L, respectively. A direct correlation exists between clinical symptoms and blood level of lidocaine; as the level increases to 8-12 mg/L the probability of seizure increases. The extent of absorption and bioavailability after airway administration depends on tissue vascularity, sites and techniques of application, patient's disease state, and, most important, the dose/unit body weight. The lidocaine dose should be titrated slowly and patients monitored for altered mental status. The dose often has to be decreased empirically in patients with liver disease or CHF. Efforts should be made to deliver minimum amounts of the drug to the lower respiratory tract, since its pharmacokinetics at that site are similar to those with intravenous administration.
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PMID:Seizure after lidocaine for bronchoscopy: case report and review of the use of lidocaine in airway anesthesia. 843 71

National and international societies have issued guidelines on the management of heart failure: The European Society of Cardiology, WHO, ACC/AHA Task Force Report, US Department of Health and Human Services, German Society of Cardiology. The therapeutic approaches to heart failure have undergone considerable changes during the last few years. The guidelines have to be updated almost yearly due to new results from prospective randomized studies. Although an agreement could be reached with respect to general measures and drug treatment, no agreement on mechanical devices, pacemakers and surgical interventions has been reached. The basis for medical treatment of chronic heart failure depends on diuretics, digitalis, ACE inhibitors, and beta-blockers. Calcium antagonists and other positive inotropic drugs, other than digitalis, should be avoided as far as possible. Thiazides, loop diuretics and aldosterone antagonists are needed for acute and chronic treatment of heart failure, alone or in combination (diuretic resistant heart failure!). Digitalis glycosides are needed in patients with atrial fibrillation with a fast ventricular rate or atrial flutter and in patients with systolic dysfunction, large hearts and symptomatic failure class NYHA III and IV. However, digitalis does not convert atrial fibrillation to sinus rhythm. Today there is no question that ACE inhibitors improve the prognosis of all patients with heart failure in all stages, if ejection fraction is reduced. Therefore, most patients after myocardial infarction or after having experienced pump failure due to myocarditis or cardiomyopathy are treated with ACE inhibitors and diuretics. The beneficial effects of ACE inhibitors seem to be most pronounced the worse the situation is. Relative risk reductions (mortality!) between 10% and 40% have been published depending on the severity of symptomatic left ventricular dysfunction. Those patients with high absolute risk have more to gain than those with low risk for any given "risk reduction", of course. Recent studies also indicate that most high risk cardiac patients profit from ACE inhibitors even if pump function is normal (i.e., patients with coronary heart disease, diabetes mellitus, cerebral vascular disease, hypertension) (15). AT1 antagonists can substitute for ACE inhibitors, if the latter are not tolerated due to cough. Up to now, beta-blocking agents apart from diuretics seem to be the best investigated drugs in heart failure. Large controlled studies with bisoprolol, carvedilol and metoprolol in addition to diuretics, digitalis and ACE inhibitors convincingly yielded positive results in chronic left ventricular failure patients. Reduction of mortality by 35% and even of sudden cardiac deaths by 40% have been proven beyond doubt. Thus, heart failure patients today should also receive beta-blocking agents in all stages of the disease. In the era of controlled prospective studies (evidence-based medicine), physicians are well advised to use only drugs that have been proven beneficial in large controlled studies.
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PMID:The management of heart failure--an overview. 1119 49

The most commonly associated anomalies in patients with extrahepatic biliary atresia are cardiovascular, digestive and splenic defects. Of the cardiovascular anomalies, there are very few reports of biliary atresia with cardiomyopathy. We report the first case of a child with extrahepatic biliary atresia and restrictive cardiomyopathy. The patient was a 13-month-old boy diagnosed with extrahepatic biliary atresia at the age of 2 months, when he underwent laparotomy for definite diagnosis.Hepatic portoenterostomy was performed after confirmative cholangiogram. Recently, he developed severe cough and dyspnea, and his respiratory symptoms worsened. Chest radiograph showed cardiomegaly. Two- dimensional echocardiography showed marked biatrial enlargement. On M- mode echocardiogram, a slight increase in left ventricular dimension was seen in early diastole with a relatively good left ventricular function. Mitral inflow Doppler tracing showed an increased E-velocity (1.1 m/sec) with decreased deceleration time (75 m/sec), and increased E/A ratio (0.33). He was diagnosed as having restrictive cardiomyopathy with characteristic echocardiographic features.
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PMID:Restrictive cardiomyopathy in a patient with extrahepatic biliary atresia. 1141 Jul 2

Cardiovascular disease is the major cause of morbidity and mortality in Westernised societies. It is well known that the aetiology of this devastating disorder involves both genetic and environmental factors. Sequence variants of the components of the renin-angiotensin-aldosterone system and the kallikrein-kinin system are suggested to have significant influences on cardiovascular homeostasis. Both gene targeting and transgenic studies in mice have clearly suggested a critical role of the angiotensin converting enzyme (ACE) gene in blood pressure regulation. Furthermore, an up-regulation of myocardial ACE gene expression has been observed in patients with heart failure. Thus, the ACE gene has been recognised as a top candidate gene for cardiovascular research. Over the past decade, the insertion/deletion (I/D) polymorphism of a 287-bp Alu element in intron 16 of the ACE gene has attracted significant attention and has been extensively investigated in a spectrum of cardiovascular phenotypes, because of its correlation with serum ACE activity. A large majority of previous studies have shown a positive association between the DD genotype and an increased risk of myocardial infarction, but results in hypertension, left ventricular hypertrophy, cardiomyopathy and restenosis after percutaneous transluminal coronary angioplasty remain quite controversial. Since ACE inhibitors are widely used in hypertension and congestive heart failure, we also review the literature on the relationship of ACE I/D polymorphism with ACE inhibitor response. It appears that this polymorphism has some moderate impact on the cardiovascular response to ACE inhibitors but there is no consensus as to which allele confers a more pronounced effect. In addition, previous data are suggestive of an association between the ACE I allele and a greater risk of increased occurrence of ACE inhibitor-induced cough, but such a relationship needs further confirmation. Overall, since ACE I/D is only an intronic marker, the true locus that controls the ACE enzyme activity remains to be identified, and could be located within either the ACE gene or another nearby gene such as the human growth hormone gene. We note that since associations tend to vary across different gender or ethnic groups, or across different socio-ecological settings, consideration of potential gene-gene and gene-environment interactions should be made. Furthermore, the dissection of the genetic underpinning of cardiovascular disease needs delineation of all molecular variants of the key physiological pathways that influence cardiovascular function.
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PMID:Angiotensin converting enzyme gene insertion/deletion polymorphism and cardiovascular disease: therapeutic implications. 1198 86

Dominant mutations in the CIAS1 gene cause a spectrum of autoinflammatory diseases such as familial cold autoinflammatory syndrome, FCAS, which is characterized by episodes of urticaria, arthralgia, fever and conjunctivitis after generalized exposure to cold. We here describe patients of two German families with the 592G-->A, V198M mutation, which has been described to induce FCAS before. However, in our patients the clinical phenotype was very different from this disease. They never had urticaria, cold induced fever or conjunctivitis; instead the following symptoms occurred: Very regular periodic fever, irregular severe febrile episodes, relatively mild arthralgia, dry cough, cardiomyopathy, nephropathy and euthyroid thyroiditis all being reversible. We conclude that the clinical phenotype associated with mutations in the CIAS1 gene is much broader than assumed before.
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PMID:Periodic fever, mild arthralgias, and reversible moderate and severe organ inflammation associated with the V198M mutation in the CIAS1 gene in three German patients--expanding phenotype of CIAS1 related autoinflammatory syndrome. 1524 11


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