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

The author presents a retrospective and complex pathomorphological analysis in 152 autopsy cases. Death was caused by different forms of cardiomyopathies. Aim of the study to reveal the frequency of pathology, causes and mechanisms of death. The prevailing frequency of dilated cardiomyopathy was established--106 cases, 0.88%. Hypertrophic and restrictive forms--32 (0.27%) and 14 (0.12%) of cases. the dominating cause of death (42.7%) was chronic cardiac failure. Other death causes were as follows: thrombosis and embolism--17.8%; arrhythmic collapse--13.2%; ventricular fibrillation--9.9%; acute left-ventricular failure--8.6%; real cardiogenic shock--7.8% of all cases of cardiomyopathies.
 ...
PMID:[The causes and mechanisms of death in cardiomyopathies]. 228 61

We studied the effects of the antianginal drug carbocromen (4 mg/kg bolus plus 80 micrograms/kg/min i.v.) on amitriptyline (400 micrograms/kg/min i.v.) toxicity. In anesthetized dogs, amitriptyline increased heart rate, left ventricular (LV) end-diastolic pressure, and the PR and QT intervals, the QRS complex, and the S-T segments of the peripheral electrocardiogram. Blood pressure, LV pressure, and LV dP/dtmax fell considerably. Survival time was 37 +/- 4 min in amitriptyline-treated dogs and 64 +/- 3 min (p less than 0.05) in those receiving amitriptyline plus carbocromen. The amount of amitriptyline consumed until death increased from 14.8 to 25.6 mg/kg (p less than 0.05) with carbocromen. In conscious dogs, the hemodynamic impact of intraatrial amitriptyline was similar to that in anesthetized animals, and changes in stroke volume resembled those of dP/dt. Cardiac output was not altered, and peripheral resistance decreased moderately. Carbocromen prevented most of the typical amitriptyline effects on the heart and circulation. Sustained ventricular arrhythmia occurred at 29 +/- 4 min with amitriptyline infusion but was delayed to 58 +/- 3 min (p less than 0.05) when carbocromen was added. These experiments demonstrate (a) amitriptyline intoxication produced ventricular tachyarrhythmia and cardiac failure if high agent concentrations were achieved; (b) these rhythm disorders were associated with slowing of intraventricular conduction, which could be enhanced by carbocromen; and (c) carbocromen might be an effective therapy for amitriptyline-caused arrhythmia with cardiovascular collapse.
 ...
PMID:Cardioprotective effects of carbocromen in awake and anesthetized dogs with amitriptyline poisoning. 241 Jul 6

Twenty patients aged 55 +/- 16 years with 40 chronic ventricular tachycardias (VT) refractory to 4.6 +/- 1.9 antiarrhythmic drugs, used alone or in combination, were managed by low doses of beta-blocker agents combined with oral amiodarone (Am), either after loading (1.2 g for 7 days, n: 5) or reloading (1.2 g for 4 days, n: 15) of Am. All patients proved refractory to Am alone. Seven VT were also refractory to endocardial catheter fulguration in six patients. Thirteen patients had coronary artery disease, three had arrhythmogenic right ventricular dysplasia, two had dilated cardiomyopathy, one had valvular disease, and one had no structural heart disease. Ten patients had an EF less than 30%. Ten patients were in NYHA functional class three. VT was permanent in three patients, daily in three, weekly in seven, paroxysmal in seven. In 11 patients, VT occurred both at day and night. In 11 patients, decrease of the sinus cycle preceeded VT. Oral administration of a daily low dose of a beta blocker agent (acebutolol 100 mg, betaxolol 5-10 mg, metoprolol 50 mg, nadolol 20-40 mg, pindolol 2.5 mg, propanolol 30 mg, sotalol 80-160 mg, terta-tolol 2.5 mg) combined with 400 mg/day of Am suppressed VT episodes in all patients. None presented heart failure or collapse. The mean reduction of the heart rate was 15% (65 to 55/min). At discharge, exercise ECG (n: 14) induced non sustained VT in two patients. At programmed electrical stimulation (PES) (n: 15), VT was no longer inducible in 4 patients, was slower, well-tolerated in nine patients, and remained inducible at the same rate in only two patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Efficacy and safety of low doses of beta-blocker agents combined with amiodarone in refractory ventricular tachycardia. 246 76

Thirty one patients aged 56 +/- 16 years with chronic ventricular tachycardias (VT) refractory to 4.4 +/- 1.8 antiarrhythmic drugs, used alone or in combination, were managed by low doses of beta-blocker agents combined with oral amiodarone, either after loading (1.2 g for 7 days, n : 7) or reloading (1.2 g for 4 days, n : 24) of amiodarone. All patients proved refractory to amiodarone alone. Nine VT were also refractory to endocardial catheter fulguration in 8 patients. Twenty one patients had coronary artery disease, 4 had arrhythmogenic right ventricular dysplasia, 4 had dilated cardiomyopathy, 1 had valvular disease, and 1 had no structural heart disease. Twelve patients had an ejection fraction less than 30 p. 100. Ten patients were in NYHA functional class 3. VT was permanent in 3 patients, daily in 5, weekly in 7, paroxysmal in 16. In 14 patients, VT occurred both at day and night. Oral administration of a daily low dose of a beta-blocker agent (acebutolol 100 mg, betaxolol 5-10 mg, metoprolol 50-100 mg, nadolol 20-40 mg, pindolol 2.5 mg, propranolol 30 mg, sotalol 80-160 mg, tertatolol 2.5 mg) combined with 400 mg per day of amiodarone suppressed VT episodes in all patients. None presented heart failure or collapse. The mean reduction of the heart rate was about 17 p. 100. One patient need a definite pacemaker to correct sinus bradycardia. At discharge, exercise ECG (n: 20) induced non sustained VT in 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Efficacy of the combination of low doses of beta-blockers and amiodarone in the treatment of refractory ventricular tachycardia]. 257 26

FeSO4 0.1-0.7 mmol/L shortened the action potential duration, decreased the action potential amplitude (APA) and maximal upstroke velocity of 0 phase (Vmax), and reduced the contractile force of myocardium in a concentration-dependent manner. FeSO4 0.2 mmol/L depressed the APA and Vmax of papillary muscles in Tyrode's solution containing MnCl2 3 mmol/L, and reduced the APA, Vmax and duration of slow action potentials in potassium-depolarized papillary muscles. These results suggest that Fe2+ may inhibit the transmembrane movement of Ca2+ and Na+ in myocardial cells. This may be one of the mechanisms of heart failure and circulatory collapse in acute iron poisoning.
 ...
PMID:[Effects of FeSO4 on electrical and mechanical activity of guinea pig papillary muscles]. 264 50

The phrase 'heart failure' is used as a shorthand by medical practitioners to describe a wide variety of medical conditions ranging from acute heart failure with pulmonary oedema to terminal chronic heart failure. The medical treatment of these entities varies widely and is dependent on an understanding of the haemodynamics, pathophysiology and aetiology of the conditions, and on the pharmacology of the drugs selected. Important distinctions should be made between systolic and diastolic, acute and chronic, and extracellular and cellular heart failure. Drugs often used for treatment include diuretics, angiotensin-converting enzyme (ACE) inhibitors, nitrates and digoxin. Pure positive inotropic drugs are of value in the treatment of circulatory collapse, post-operatively and in terminal heart failure. Drugs with a mild positive inotropic effect which also possess other properties such as systemic vasodilation, renal vasodilation and alteration of diastolic function may be of wider value in the treatment of mild to moderate chronic heart failure but that prediction awaits proof from controlled clinical trials.
 ...
PMID:Relevance of the aetiology of heart failure to drug therapy. 268 Apr 94

Calcium blockers (CB) are routinely used. This could lead to possible interference with anaesthetic drugs. CB prevent calcium from entering the cell by inhibiting the slow voltage-dependent calcium channels. They act mostly on heart and smooth muscle. Of all the possible indications, the three that are confirmed are coronary heart disease, arterial hypertension and supraventricular rhythm disturbances. Most of the work published and the cases reported concerns interactions between CB and halogenated anaesthetic agents; the latter's actions on the heart depend on cellular calcium exchange. Also, the cardiovascular effects of these anaesthetics are similar to that of CB. Experimentally, halothane and enflurane have direct cardiac inhibitory effects similar to verapamil and diltiazem, whereas isoflurane's properties seem closer to the dihydropyridines (nifedipine and nicardipine). Giving verapamil or diltiazem increases the number of sino-atrial and atrio-ventricular blocks when using a halogenated agent. Clinically, interpreting the effects of CB during anaesthetic induction is difficult because of the pathology (coronary heart disease, cardiac failure), the other drugs (beta-blockers and nitrates) and the type of anaesthesia (emergency or elective). Interactions can give rise to anything from a severe cardiovascular collapse, requiring catecholamines, to a mild fall in blood pressure which responds well to plasma expansion, or even no effect on blood pressure. Rebound is seen on stopping CB in patients with coronary heart disease or arterial hypertension; stopping them before surgery does not therefore seem justified. However, extreme care must be taken when using halogenated agents for patients under treatment with CB and/or beta-blockers. A wary anaesthetist will be able to adapt the technique to the patient. It has been suggested that CB could be used to treat preoperatively myocardial ischaemia (diltiazem), hypertensive crises (nifedipine, nicardipine) and ventricular rhythm disturbances (verapamil); this must be done with caution, the patient being closely monitored (haemodynamic and electrocardiographic monitoring). Postoperatively, intranasal nifedipine, continuous intravenous nicardipine or diltiazem have been used to treat increases in arterial blood pressure during recovery and to adapt the cardiovascular system to the increased metabolic needs. Here again, close patient monitoring is essential. In any case, treatment with CB which has been stopped should be started up again as soon as possible.
 ...
PMID:[Calcium inhibitors and anesthesia]. 297 26

A naturally occurring cardiomyopathy in broiler chickens from a single Ontario farm was studied in order to define the morphologic changes. Gross and histologic features of affected birds were compared with those in age-matched control penmates. Body weight and weight and volume of individual cardiac chambers were measured. Histologic sections of 18 different tissues were examined, and lesions observed were scored subjectively. Affected birds were stunted and had marked right ventricular dilation and hypertrophy, atrial hypertrophy, ascites, pulmonary congestion and edema, and hepatic capsular fibrosis. Microscopic changes in the heart of affected birds were mild and did not suggest a specific cause of heart failure. Lungs had marked hypertrophy of parabronchial smooth muscle and collapse and apparent loss of associated air capillaries. Other histologic changes observed were thought to be the result of passive congestion of viscera caused by right heart failure and chronic debility. Although the specific etiology of this condition could not be determined, it was felt that this syndrome was unlikely to have been the result of any of the commonly recognized causes of congestive heart failure and ascites in broilers.
 ...
PMID:Lesions of right heart failure and ascites in broiler chickens. 304 56

Hunter's disease is a genetically transmitted defect known to produce mucopolysaccharide infiltration of multiple organ systems. Upper airway obstruction is caused by an enlarged tongue, deformed pharynx, and short, thick neck. Its eventual lethal outcome by the second decade of life is known to result from an infiltrative cardiomyopathy leading to irreversible heart failure. Instead, our recent experience in the care of five patients with this disorder suggests the lethal event is related to progressive obstruction sequentially involving the upper, mid, and lower airway characterized by gradual deformation and collapse of the trachea. Autopsy and histopathologic whole organ sections demonstrate anteroposterior flattening of the trachea and bronchi with submucosal thickening producing structural alterations known only to this disease.
 ...
PMID:Hunter's syndrome: a study in airway obstruction. 310 69

Phrenic nerve palsy (PNP) is seen in infants and young children usually resulting from operative trauma or birth injury. Spontaneous recovery usually occurs, but occasionally surgical plication is necessary. Twenty-three cases of PNP over a 10-year period were managed surgically. Patient ages ranged from 1 day to 30 months (median, 4 months), 18 were male and five female. Cause was operative trauma in 18 (17 cardiac surgery, one neuroblastoma), birth trauma in two, and idiopathic in three. The right side was involved in 14, the left in eight, and both in one. Indications for plication were inability to wean from the ventilator (group 1, 16 patients), recurrent pneumonia (group 2, four patients), and respiratory distress (group 3, three patients). The 16 patients in group 1 were intubated for a median of 18.5 days from onset of PNP to plication. Postoperatively, three had continuing congestive heart failure (one died at 16 days of age, one was still chronically ventilated at 22 months, one was extubated at nine days); the other 13 were extubated at a median of two days postoperatively. All the patients in groups 2 and 3 were extubated within two days of surgery. Twelve plications were transthoracic and 11 were transabdominal. Postoperative complications included pneumonia (2), wound infection (1), pneumothorax (2), and mucous plug with pulmonary collapse (1). One patient died of cardiac failure at 16 days. One patient in group 3 developed recurrent respiratory distress 4 months postoperatively; he had a recurrent elevated hemidiaphragm requiring a second plication.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Plication of the diaphragm for infants and young children with phrenic nerve palsy. 317 45


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>