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)

Acute heart failure is a life-threatening medical emergency, most commonly occurring as an immediate or delayed complication of acute myocardial infarction (AMI), or resulting from severe hypertension or valvular defects (stenosis or incompetence). Occasionally it is caused by patients' non-compliance with medication orders. In this case the patient had a history of three previous AMIs, controlled hypertension, and controlled congestive heart failure (CHF) for which he took two 40 mg frusemide tablets (a very potent oral diuretic) each morning. Because he had experienced bladder discomfort during the latter stages of previous appointments he decided to delay taking the diuretic until after his appointment and acute heart failure ensued.
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PMID:A case report of acute heart failure caused by a patient delaying taking his diuretic medication. 1203 61

A Japanese man who died at age 85 had been followed since the age of 59, when he first presented. He had hypertension of 162/102 mmHg and a loud systolic murmur on his first visit. He had had an active daily life without any medication for the next 10 years. At the age of 72 he complained of mild chest discomfort on exercise. Although electrocardiography showed no abnormalities, echocardiogram showed calcified bicuspid aortic valve with mild stenosis. At the age of 81 the dyspnea and chest oppression were exacerbated, associated with marked ST depression on exercise electrocardiogram and restriction of aortic valve opening on echocardiograms. In the following years a gradual increase in QRS voltage and ST depression with T wave inversion were recorded on resting electrocardiograms and sharp increases in both left ventricular end-diastolic diameter and flow velocity at the aortic root were observed on echocardiograms. At the age of 85 he died of intractable heart failure with massive pleural effusion. Autopsy revealed marked hypertrophy and moderate dilatation of the heart (weight: 580 g). The bicuspid aortic valve had anterior-posterior cusps with a raphe on the anterior cusp. The mobility of the cusps was almost lost because of severe calcification and thickening. Severe stenosis was found near the orifice of the right coronary artery, but there were no significant ischemic myocardial lesions.
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PMID:[An autopsied case with a bicuspid aortic valve who had progressive angina pectoris and heart failure during follow-up of 27 years]. 1218 11

The present study was aimed at determining the frequency and circadian variations in symptomatic or silent myocardial ischemia in ambulatory patients with stable coronary disease. A comparative analysis was then made of the recordings on symptomatic and asymptomatic patients according to their medical history. Three hundred and twenty-one cardiologists recruited a total of 1,088 patients who were monitored for 4 days with a new type of electrocardiographic recorder. The patients were able to voluntarily start up the recorder in the case of cardiac discomfort or pain. The results showed that over a total recording period of 95,725 hours, the following data, which were validated by an experienced cardiologist, were obtained: 3,258 ischemic episodes, 2,963 (or 91%) of which were cases of silent ischemia, and 295 (or 9%) which were symptomatic. All the ischemic episodes involved a limited number of subjects, i.e., 271 patients. Of these, 148 (54.6%) were completely asymptomatic; only 63% of these patients with silent ischemia would have been detected if the recording had just lasted 24 hours. Moreover, the medical history showed a correlation between certain factors (such as poorly managed arterial hypertension, cardiac insufficiency, renal failure, arteritis of the lower limbs, and a waist-hip relation of over one in men) and an increase in the number of cases of silent ischemia. However, no single factor was found to be linked more to silent ischemia than to symptomatic ischemia. This investigation therefore shows the significant numeric incidence of silent ischemia. It raises the question of the need to prescribe treatment in at-risk subjects which includes recordings of long duration, so that silent ischemia, which may increase the risk of mortality, can be more readily detected.
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PMID:[Frequency of silent and painful ischemia in patients with treated stable coronary insufficiency]. 1255 11

Dissection of the coronary sinus during lead implantation for biventricular pacemaker implantation in patients with advanced heart failure is a serious complication that has occasionally been reported. We report on the clinical outcome and angiographic follow-up in a series of 7 patients with acute major dissection from 103 consecutive attempts (incidence 6.8%). Serial echocardiography was performed in all patients and all underwent follow-up angiography 2-3 months after the procedure. In 1 patient, pericardial extravasation was seen during retrograde venography. Clinical follow-up was uneventful except for one other patient who complained of prolonged chest discomfort for several hours after the procedure. In none of the patients were there signs of pericardial effusion or tamponade demonstrated on echocardiography. Venograms during the procedure and after follow-up were analysed using a quantitative coronary angiography system (CAAS II). Parameters included minimal luminal diameter, diameter stenosis, minimal cross-sectional area and an estimation of the reference diameter. There were no significant differences in all analysed parameters, although in 1 patient a small partial dissection was present. Thus, although dissection of the coronary sinus following lead implantation for biventricular stimulation is not an uncommon complication, it is usually well tolerated. Long-term angiographic follow-up demonstrated no significant vessel damage or vessel remodeling.
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PMID:Major dissection of the coronary sinus and its tributaries during lead implantation for biventricular stimulation: angiographic follow-up. 1469 25

Noncardiogenic pulmonary edema, and, to a lesser extent, acute respiratory distress syndrome (ARDS), are common clinical manifestations of drug-induced lung diseases. Clinical features and radiographic appearances are generally indistinguishable from other causes of pulmonary edema and ARDS. Typical manifestations include dyspnea, chest discomfort, tachypnea, and hypoxemia. Chest radiographs commonly reveal interstitial and alveolar filling infiltrates. Unlike pulmonary edema that is due to congestive heart failure, cardiomegaly and pulmonary vascular redistribution are generally absent in cases that are drug-related. Rare cases of drug-induced myocarditis with heart failure and pulmonary edema have been described. Results from laboratory evaluation and respiratory function tests are nonspecific.
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PMID:Drug-induced pulmonary edema and acute respiratory distress syndrome. 1506 1

The concept of analgo-sedation in intensive care medicine has changed considerably since the last decades. Deep sedation, keeping patients artificially unconscious, is not necessary anymore, it postpones weaning from mechanical ventilation, it provokes complications, and prolongs the length of ICU stay. On the other hand, recent surveys have shown that patients recall their intensive care experience still as stressing and painful. This need more awareness of patient's pain and the readiness to give analgesics particularly before painful procedures. The frightening environment of the ICU, sleep deprivation, pain and discomfort related not only to the actual dysfunctions, but even more to the stressing procedures of care and treatment, make a certain level of sedation necessary. But patients' discomfort may also originate from many other reasons, such as hypoxaemia, hypotension, cardiac failure, drugs overdose or withdrawal, or simply from an uncomfortable body position. These sometimes non-obvious reasons have to be carefully looked for in order to treat the problem effectively. Delirium and other mental problems are common in critically ill patients. They have to be diagnosed with particular attention and treated specifically. Sedatives must be carefully adapted to the individual needs and the actual situation. Modern modes of mechanical ventilation allows lower levels of sedation. Regularly repeated assessment of the sedation level (e.g. by Ramsay score) is mandatory; a sedation protocol seems advantageous. To avoid inadvertent accumulation and overdose, it is recommended to keep the patient at a sedation level at which communication is still possible. A daily interruption of the sedation has shown to shorten the duration of mechanical ventilation and the length of ICU stay.
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PMID:Aims of sedation/analgesia. 1621 Sep 98

Congestive heart failure is an increasingly common condition carrying a poor prognosis and a decay in the quality of life. Usually frequent and lengthy hospitalizations are required with heart failure, with obvious discomfort for the patient and increase in health costs. Heart transplantation is rarely possible due to shortage of donors. Thus, improvement of pharmacological strategies for the management of these patients is desirable. The present study evaluated the effects of intermittent dobutamine infusion in elderly patients (mean age 75.9 years), hospitalized for advanced (NYHA, 1973, class IV) congestive heart failure of ischemic etiology. Dobutamine infusions of 2, 4 and 6 microg/kg/min for 36 h every 2-4 weeks were randomly prescribed to 24 subjects, who were then followed up every three months for an average of ten months. Data on mortality, cardiovascular events and NYHA (1973) functional classifications were systematically collected. Our study shows that while in this series of patients mortality remained high (50% at 12 months), there was an improvement in the NYHA-classification during the follow-up, and a decrease in the need for hospitalization. In addition, side effects were relatively rare, with only two patients interrupting dobutamine treatment. We conclude that intermittent dobutamine infusion is a reasonable treatment option in elderly patients with congestive heart failure unresponsive to conventional treatments.
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PMID:Intermittent dobutamine therapy in patients with advanced congestive heart failure. 1537 51

A 53-year-old man was admitted to Keio University Hospital because of serious dyspnea and edema of the lower extremities. Eighteen months previously, the patient had complained of chest discomfort, and was then admitted for the first time to our hospital for evaluation of chest pain. Electrocardiography showed poor R wave progression in leads Vl through V4, and diffuse nonspecific ST-segment and T wave abnormalities with low voltage. However, no definitive diagnosis could be made at this initial admission and a calcium-channel blocker was prescribed. Despite this treatment, the patient was readmitted with worsening dyspnea and lower extremity edema. The diagnosis of heart failure and nephritic syndrome was made at the second admission. In addition, immunoelectrophoresis showed a monoclonal IgD (lambda) M protein and increased plasma cells in the bone marrow, suggesting a diagnosis of multiple myeloma. The patient was thus given dexamethasone (20 mg per day for 4 days) intravenously, but his symptoms did not improve. Two weeks later, the patient deteriorated further with congestive heart failure and renal failure, and subsequently died of cardiac arrest with ventricular fibrillation. On autopsy, IgD (lambda)-positive plasma cell proliferation was found in the bone marrow, confirming the diagnosis of multiple myeloma. In addition, amyloid deposition was detected in various organs including the heart, kidneys, esophagus, duodenum, ileum, colon, tongue, and lungs. In particular, the weight of the heart was 650 g demonstrating a hypertrophic septum and amyloid deposition in the myocardium and even coronary arteries. In summary, the final diagnosis was IgD (lambda) multiple myeloma associated with systemic amyloidosis.
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PMID:IgD myeloma with systemic amyloidosis with chest discomfort as an initial symptom. 1547 32

Venous thromboembolism, which is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE), represents a significant cause of death, disability, and discomfort. Two million people/year are affected by VTE, making it the third most common cardiovascular disease after coronary heart disease and stroke. The rationale for VTE prophylaxis stems from the clinically silent presentation of the disease and its prevalence among hospitalized patients. At greatest risk are patients undergoing major orthopedic surgery and those admitted to the intensive care unit with acute myocardial infarction, heart failure, ischemic stroke, respiratory disease, systemic infection, or other medical conditions that immobilize patients for 5 days or longer. Several anticoagulant regimens have been effective in reducing the risk of VTE after major orthopedic surgery. For patients undergoing total hip or knee replacement, treatment with adjusted-dose warfarin, low-molecular-weight heparins, or fondaparinux may be used. Warfarin, which has been around for more than 50 years, is the only oral anticoagulant available for VTE prophylaxis. Ximelagatran, a new low-molecular-weight oral prodrug of the direct thrombin inhibitor melagatran, has advantages over warfarin that may make it the drug of choice for prevention of VTE.
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PMID:The role of oral direct thrombin inhibitors in the prophylaxis of venous thromboembolism. 1562 37

Atrial fibrillation is the most commonly sustained cardiac arrhythmia and a common reason for mortality and morbidity. Atrial fibrillation causes disease for three reasons: i) the ventricular rate is often high, which leads to symptoms ranging from discomfort to life threatening heart failure; ii) the rhythm causes loss of atrioventricular synchrony, which reduces diastolic filling and may lead to heart failure; and iii) atrial contraction is lost leading to stagnant blood that again may lead to atrial thrombi and peripheral embolism. Thus, the treatment of atrial fibrillation is focused on the maintenance of sinus rhythm, rate control and prevention of embolism. For the maintenance of sinus rhythm, all drugs under current development are potassium channel blockers; the so-called class III anti-arrhythmic drugs. Those which have been further investigated appear to be valuable for maintenance of sinus rhythm but all carry a significant risk of pro-arrhythmia, in particular Torsade de Pointe ventricular tachycardia. Rate control has been a focus of treatment for many years and several very old drugs, including digoxin, are used for this. There is, to the author's knowledge, no current effort for evaluating new drugs for this indication. Prevention of embolism has for many years been obtained with vitamin K antagonists for which the clinical evidence is overwhelming. Previous attempts to replace vitamin K antagonists with aspirin have not been fruitful. A large number of newer anticoagulation regimes are in development, but to the author's knowledge only a single thrombin inhibitor is actively being developed for atrial fibrillation.
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PMID:The immediate future for the medical treatment of atrial fibrillation. 1598 49


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