Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess the clinical efficacy of a combination of penicillin G and ofloxacin in the treatment of community acquired pneumonia. Thirty eight patients (23 males, 15 females, mean age 62.8 years +/- 19.6) were included. They presented a CAP with the following criteria: fever, abnormal chest X-ray pattern. They received the combination of IV penicillin 12 x 10(6) U daily and IV ofloxacin 200 mg bid. After 48 hours of apyrexia, this treatment was followed by oral ofloxacin alone 200 mg bid. In six cases, the etiologic agent was identified: 2 S. pneumoniae, 1 Chlamydiae psittaci, 2 Staphylococcus aureus, 1 Mycoplasma. In 32 cases, the bacteriological investigation was negative. Five patients were excluded: 2 deaths due to heart failure, 3 alterations of treatment. Twenty eight patients recovered: apyrexia was obtained in 3.5 days. Penicillin G was prescribed for 7.5 days +/- 2.65, followed by ofloxacin alone for 11.43 +/- 3 days. Five patients were considered as clinical failures: 2 deaths due to extensive pneumonia, 3 recoveries after alteration of treatment. Side effects were rare: 1 confusion, 2 skin rashes. As a conclusion: penicillin G and ofloxacin in combination for the initial therapy of CAP, rapidly relayed by ofloxacin alone, permitted 84.3% of recovery in our patients.
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PMID:[The combination of penicillin G and ofloxacin: a response to the empirical treatment of community acquired pneumonia]. 238 49

Since most of the toxicity associated with class 1B antiarrhythmic drugs is dose-related, this review examines adverse effects seen in both therapeutic practice and accidental or premeditated overdose. Toxicity is very common with these agents and can be life-threatening. A high percentage of patients must discontinue therapy because of adverse effects. Mexiletine and tocainide are structural analogues of lignocaine (lidocaine) and toxicity is similar with all 3 drugs. With gradual intoxication (the most common form) central nervous system effects such as lightheadedness, dizziness, drowsiness and confusion are seen first. Seizures and respiratory arrest can occur. Cardiovascular toxicity is manifested by progressive heart block, reduced cardiac contraction, hypotension and asystole. Both mexiletine and tocainide may have proarrhythmic effects. Gastrointestinal toxicity is also common. Shock, hypotension, cardiac failure and beta-blocker therapy reduce lignocaine clearance and enhance the risk of intoxication during routine therapy. Both lignocaine and mexiletine elimination is impaired in severe liver disease while tocainide clearance is reduced in renal failure. Management of toxicity is largely supportive and symptomatic. Lignocaine infusion must be discontinued and decontamination of the gut in the case of oral preparations is recommended. Serious intoxication requires intensive care unit admission. Haemodialysis or haemoperfusion may be helpful in serious lignocaine and tocainide poisoning. In institutions where extracorporeal circulatory assistance is available, massive lignocaine poisoning has been successfully treated with this intervention. In the therapeutic setting serious toxicity can be prevented by close clinical surveillance and appropriate dose reduction in patients with reduced drug clearance. Because of the large interindividual variation in lignocaine pharmacokinetic parameters, therapeutic drug monitoring is recommended if results can be reported quickly. Mexiletine and tocainide have stereoselective metabolism and assays do not distinguish the more active isomers. Therapeutic drug monitoring is less useful in this situation.
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PMID:Poisoning due to class 1B antiarrhythmic drugs. Lignocaine, mexiletine and tocainide. 251 64

We have introduced enalapril, in doses equal to or less than the 2.5 mg currently recommended, as an adjuvant to digoxin and diuretics in 17 patients of mean (SD) age 83 (5) years with severe heart failure. Only eleven patients tolerated its introduction. Unlike those reported in younger patients, all but one of the adverse drug reactions occurred 8 h or more after the first dose. Aged patients started on ACE inhibitors should be observed in hospital until stabilized on a maintenance dose. Three patients had an adverse reaction which differed in nature from those previously reported: acute confusional state, ataxia and mesenteric ischaemia. Ten patients were discharged on 5 mg or 10 mg maintenance doses of enalapril. In nine of them improvement on triple therapy was sustained for a minimum of three months. ACE inhibition was lost in the other patient when her compliance with enalapril therapy fell to around 75%: monitoring compliance is essential when ACE inhibitors are used in low dosages. Enalapril was withdrawn during follow up in three patients because of symptoms of mesenteric ischaemia and in four because of dramatic deterioration of renal function. One of the latter was found subsequently to have severe bilateral atheromatous renal artery stenosis. When isosorbide dinitrate was substituted for enalapril, symptoms of mesenteric ischaemia resolved and renal function returned to baseline. Continuing surveillance for adverse effects is essential in patients of this age group with severe heart failure, and the risk of occult renal artery stenosis requires regular biochemical screening during follow up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of the safety of enalapril in the treatment of heart failure in the very old. 284 29

Passive liver congestion secondary to increased hepatic venous pressure may accompany congestive heart failure. Abnormal patterns of hepatic parenchymal contrast medium enhancement in 25 patients with advanced congestive heart failure who were studied with computed tomography (CT) include a lobulated, patchy, inhomogeneous pattern in all 25 patients, an irregular perivascular enhancement in 14, and a global delay in parenchymal enhancement in nine. CT examinations showed cardiomegaly in the 20 patients with cardiac failure and pericardial effusion or thickening in the five patients with pericardial disease. Also noted were distention of the inferior vena cava (IVC) in 24 patients, hepatomegaly in 23, early reflux of contrast medium into the IVC in 21 and hepatic veins in 16, and hepatic perivascular lymph-edema in six. The abnormal patterns are thought to be due to slowing of hepatic blood flow. Confusion with Budd-Chiari syndrome and other forms of multifocal hepatic disease is avoidable with clinical and radiologic correlation.
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PMID:Inhomogeneous enhancement of liver parenchyma secondary to passive congestion: contrast-enhanced CT. 291 31

Using bolus-enhanced CT, we encountered an unusual constellation of findings in seven patients with clinical evidence of right heart failure. These included retrograde hepatic venous opacification on the early bolus scans and a diffusely mottled pattern of hepatic enhancement seen only during the vascular phase of contrast administration. Ancillary CT findings include cardiomegaly, pleural effusions, ascites, and intrahepatic perivascular radiolucency. We believe that these CT abnormalities are caused by passive hepatic congestion. This pattern of abnormal hepatic enhancement represents a potential pitfall in the use of dynamic bolus-enhanced CT for the detection of focal hepatic masses. Recognition of passive hepatic congestion as a possible cause of mottled hepatic enhancement on CT may help explain clinical abnormalities of liver function in patients with heart failure and prevent confusion with other disease processes that produce abnormalities of hepatic attenuation.
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PMID:Passive hepatic congestion in heart failure: CT abnormalities. 326 26

The combination of nifedipine and atenolol must be evaluated in terms of risks and benefits to the hypertensive patient. Disadvantages with single-agent therapy justify trials of combination regimens. beta-Blockers may be unacceptable to some patients because of gastrointestinal upset, musculoskeletal symptoms, tiredness, malaise, insomnia, depression or confusion, sweating, breathlessness or cold extremities. The side effect profile varies from patient to patient and between different beta-blockers. Calcium antagonists also have characteristic side effects, including severe headaches, flushing and oedema, tachycardia and possibly worrying palpitations, and polyuria. Combining a calcium antagonist and a beta-blocker can reduce some side effects; for example, tachycardia is offset by addition of beta-blocker to calcium antagonist therapy, and beta-blocker-induced cold extremities may be reversed with a drug such as nifedipine. Moreover, the antihypertensive efficacy is increased, which is useful in previously resistant patients. However, an excessive fall in blood pressure is a possible adverse effect of the combination. There is also the possibility of precipitating heart failure in patients with cardiomegaly and severely compromised left ventricular function. The combination of nifedipine and atenolol was evaluated in 25 patients in a randomised, crossover trial following a month's treatment with atenolol 50mg twice daily. Patients received either atenolol 50mg twice daily alone, or atenolol 50mg twice daily with sustained release nifedipine 20mg or 40mg twice daily, or placebo twice daily during three 4-week treatment periods. Additional antihypertensive benefit was obtained by addition of the low dose of nifedipine compared with atenolol alone, but no further advantage was obtained with the higher nifedipine dose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Aims of combination therapy--improved quality of life or better blood pressure control? 337 14

To estimate the frequency of diuretic-related electrolyte disorders in the elderly, 561 consecutive admissions to three acute geriatric units were studied. For the 287 admissions to one unit, discharge/death diagnoses were also examined in relation to admission diuretic therapy. Sodium concentrations were significantly lower, and urea and creatinine significantly higher, in patients on diuretics, though the size of the differences was small. Comparing different preparations sodium concentrations were significantly lower on Moduretic than on Dyazide or Navidrex K and on frusemide when combined with a potassium-retaining diuretic rather than a potassium supplement. Potassium concentrations were significantly lower on Bendrofluazide alone compared to Navidrex K or Moduretic. Diuretics were positively associated with cardiac failure, ischaemic heart disease, airflow obstruction and obstructive large bowel disorders but negatively with Parkinson's disease. No significant association was found with falls, immobility or confusion. Major electrolyte disorders on diuretics appear to be unusual but important differences exist between preparations. Similarly major illness resulting from diuretic therapy is rare but minor morbidity may be more common.
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PMID:Biochemical and clinical correlates of diuretic therapy in the elderly. 379 65

Post mortem examinations were carried out on 52 patients who died from major burn injury from 1971-1985. Causes of death were accounted for by pneumonia and sepsis 44.2%, shock syndrome 21.2%, and cardiac failure 19.2%. The relationship between duration of survival and cause of death revealed that if the patient died in the first three days after burn injury it was usually due to "shock", if between the fourth to twentieth day then 34.6% had pneumonia and 30.8% cardiac failure. "Accidental" sepsis (46.1%) was the most frequent cause of death after three weeks. Clinical and pathological diagnosis varies between burns centers and may cause confusion. An international standardization register should be sought to permit comparison of results.
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PMID:[An analysis of clinical aspects and autopsy protocols of 52 deceased patients with burn injuries]. 380 53

Since the introduction of ophthalmic timolol solution in 1978 there have been numerous reports of systemic toxicity associated with its use. The majority of the systemic side effects reported are the same as those associated with oral timolol. Several cases of respiratory distress have been described generally in patients with underlying restrictive airway disease. Cardiovascular effects range from effects on resting pulse rate to the development of overt bradycardia and heart failure. Central nervous system effects reported include fatigue, confusion, depression, and hallucinations. A variety of other systemic effects have also been described. Caution should be used when ophthalmic timolol is administered to elderly patients or those patients with contraindications to systemic beta-blockers.
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PMID:Systemic side effects associated with the ophthalmic administration of timolol. 388 77

Calcium channel blockers are assuming increasingly important roles in the practice of emergency medicine. Two cases and a review of the literature relating to treatment of hypertensive emergencies with nifedipine are presented. Nifedipine has a rapid onset of action (buccal, 10-15 minutes; oral, 30-45 minutes) and peak effect (buccal, 30 minutes, oral, 60 minutes). The duration of effects is four to six hours regardless of the route of administration, with a mean arterial pressure reduction of 21.6% (248/134 mm Hg to 165/87 mm Hg). In patients with severe hypertension and left ventricular failure, a consistent reduction in systemic vascular resistance (2,088 dynes/sec/cm-5 to 1242 dynes/sec/cm-5) and cardiac index (2.76 l/min/m2 to 3.77 l/min/m2) has been reported. The patients in this study had severe hypertension (systolic blood pressure greater than 180 mm Hg, diastolic blood pressure greater than 120 mm Hg) and end organ involvement (including heart failure, left ventricular strain, headache, confusion, dizziness, and shortness of breath). Nifedipine (10 mg) was administered buccally with prompt reduction of blood pressure and resolution of the patients' symptoms. Nifedipine appears to be a safe, effective agent for the management of hypertensive emergencies. Its pharmacokinetic profile and routes of administration make it particularly valuable in the practice of emergency medicine.
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PMID:Nifedipine in the management of hypertensive emergencies: report of two cases and review of the literature. 406 18


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