Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cohort of 189 men was followed up for 1 year after performance of coronary angiography and determination of risk factors to ascertain which risk factors or clinical and laboratory findings could aid in predicting the patients who would have a substantial cardiac morbid event. Data on clinical signs and symptoms, psychosocial assessments, angiographic findings and presence of standard risk factors for coronary artery disease were collected in each case. Twenty-five percent of the men experienced a substantial cardiac morbid event (hospitalization, myocardial infarction, resuscitation or death). With or without inclusion of the patients who underwent surgery, discriminant analysis equations were successful in predicting morbidity on the basis of risk factor data. For the whole sample such analysis was significant at p < 0.00005 and accurately predicting the fate of 78 percent of the subjects. With exclusion of the surgically treated patients, the discriminant analysis accurately predicted future morbidity 83 percent of the time (p < 0.0001). The following risk factors for increased morbidity were common to both analyses: severity of angina, history of myocardial infarction, family history of heart disease, fatigue and absence of type A behavior.
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PMID:Predicting cardiac morbidity based on risk factors and coronary angiographic findings. 745 12

This model is used to understand the interrelationships of the physiological factors determining endurance performance ability during prolonged exercise. Early studies found that marathon runners maintain a velocity in competition that corresponds to the intensity at which lactate begins to accumulate in blood and muscle [7, 8, 19]. From this observation, the concept developed that this blood lactate threshold (LT Vo2) reflects the degree of muscular stress, glycogenolysis and fatigue. However, it was not clear whether the lactate accumulation was a result of cardiovascular limitations linked to oxygen delivery, as reflected by Vo2max [54], as opposed to metabolic factors in the exercising muscle related to the extent to which mitochondrial respiration is disturbed to maintain a given rate of O2 consumption [29, 30]. Two studies were performed to determine whether LT Vo2 was tightly coupled to Vo2max. In one study, endurance-trained ischemic heart disease patients were observed to possess a Vo2max that was 18% below that of normal master athletes who followed the patient's training program and who displayed the same performance ability as the patients. Both the patients and the normal men displayed an identical LT Vo2 (i.e., 37 ml/kg/min) (Fig. 2.5). Therefore, performance was determined primarily by LT Vo2 instead of Vo2max in this situation, albeit with abnormal subjects. In a second study we assembled two groups of competitive cyclists who were identical in Vo2max but differed by having a high or low LT Vo2 (82% vs. 66% Vo2max) [13]. When cycling at 80-88% Vo2max, the low LT group displayed more than a 2-fold higher rate of muscle glycogen use and blood lactate concentration, and as a result were able to exercise only one-half as long as the high LT group. Performance time for a given Vo2 was clearly related to LT Vo2 instead of Vo2max (Fig. 2.6). This is not to say that Vo2max plays no role in determining LT Vo2, because as in heart disease patients, it clearly sets the upper limit. Indeed, we have seen that much of the variance (i.e., 31-72%) in LT Vo2 is related to Vo2max. (Fig. 2.11.) However, improvements in performance after the first 2-3 yr of intense training are associated with improvements in LT Vo2, whereas Vo2max generally increases very little thereafter (Table 2.3). The next question concerns the factors responsible for further increases in LT Vo2 and Performance. Another major factor determining LT Vo2 is the muscle's Aerobic Enzyme Activity or mitochondrial respiratory capacity, as discussed in previous reviews [29, 30].(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Integration of the physiological factors determining endurance performance ability. 755 53

Although exercise testing has been advocated to unmask proarrhythmic potentials in patients receiving flecainide acetate, the effects of this drug on exercise parameters in individuals without structural heart disease have not been reported. This study was undertaken to assess the effects of flecainide on hemodynamics and electrocardiographic changes during exercise testing in 24 patients with paroxysmal supraventricular tachyarrhythmias, who had normal cardiac structure and sinus node function. Paired treadmill exercise tests using the Bruce protocol were performed after 1 week of treatment with flecainide (200 mg/day) or placebo in a double-blind, randomized design. Exercise testing was terminated because of either fatigue or dyspnea in all subjects. Although resting heart rate was unaffected, flecainide reduced the exercise heart rate (expressed as a percentage of age-predicted maximum) compared with placebo (84 +/- 12% vs. 92 +/- 9%, p < 0.001). Neither resting and exercise systolic blood pressure nor exercise duration were affected. PR interval shortening with exercise was not affected by flecainide, whereas QRS was prolonged compared with placebo (20 +/- 9% vs. 0 +/- 8%, p < 0.01). Compared with placebo, flecainide significantly shortened QTc (-7 +/- 12% vs. 0 +/- 8%, p < 0.05) and JTc (-34 +/- 11% vs. -21 +/- 11%, p < 0.01) intervals during exercise. During exercise, flecainide produced significant depression in the sinus node automaticity and manifested use-dependent slowing of ventricular conduction and acceleration in ventricular repolarization.
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PMID:Effects of flecainide on exercise hemodynamics and electrocardiography in patients without structural heart disease. 774 84

Growth in children with congenital heart disease (CHD) is often compromised. For several decades, investigators have tried to identify the factors affecting growth in children with CHD. Cardiac malformations are undoubtedly responsible for malnutrition, which may range from mild undernutrition to severe failure to thrive (FTT). Malnutrition may then significantly undermine the outcome of corrective surgical operations and postoperative recovery. Mechanisms linking CHD to malnutrition may be related either to decreased energy intake and/or to increased energy requirements. Decreased energy intake can involve deficiencies of specific nutrients, or insufficient total caloric intake. Increased respiratory rate accompanying congestive heart failure may be responsible for increased energy requirements. Different types of cardiac malformations and consequent interventions may have different effects on growth and require diverse strategies. Most treatment strategies aim to facilitate "catch-up" growth, providing extra calories and protein that exceed the Recommended Dietary Allowance for age. However, there is no generally accepted set of guidelines that define appropriate caloric intake for catch-up growth. We attempt to identify the most important causes of malnutrition and highlight the most effective nutrition strategies for children with CHD.
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PMID:Children with congenital heart disease: a nutrition challenge. 781 52

Health-related quality of life (HRQOL) of 166 adults who had previously undergone surgical treatment for intractable epilepsy was compared with that of outpatients with hypertension, diabetes, heart disease, and/or depressive symptoms. Eight self-reported HRQOL domains were evaluated and compared by the RAND 36-Item Health Survey 1.0: emotional well-being, social function, role limitations due to emotional problems, energy/fatigue, pain, role limitations due to physical problems, physical function, and general health perceptions. A pictorial item on overall QOL was also administered, for a total of 9 HRQOL domains. With adjustment made for age, gender, education, and comorbid conditions, 55 completely seizure-free patients scored higher (i.e., better health) than patients with hypertension in 6 of 9 domains, higher than diabetic patients in 8 of 9, higher than those with heart disease in all 9, and higher than those with depressive symptoms in all 9 (all p < 0.05). Sixty-seven patients still having seizures with impaired consciousness scored worse than hypertensive patients in 5 domains, worse than diabetic patients in 3, and worse than heart disease patients in 2; for all 3 conditions, these domains included emotional well-being and overall QOL (p < 0.05). These 67 patients, however, scored better than patients with depressive symptoms in all 9 domains, better than those with heart disease in 2, and better than those with diabetes in 1 (all p < 0.05). Forty-four other patients had only simple partial seizures (SPS); their scores were comparable to those of diabetic and heart disease patients on mental and social health scales but were higher ("better") than those of these patients on physical health scales. HRQOL among patients who have undergone "curative" epilepsy surgery is better than that of patients who have hypertension, diabetes, heart disease, or depressive symptoms. Patients who have continued seizures with altered consciousness are worse off in terms of emotional well-being and overall QOL than all other patients, except for those with depressive symptoms.
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PMID:Quality of life of epilepsy surgery patients as compared with outpatients with hypertension, diabetes, heart disease, and/or depressive symptoms. 802 6

Excess fatigue and exhaustion are among the most prevalent premonitory complaints of myocardial infarction and sudden cardiac death. These feelings may reflect subclinical heart disease, prolonged psychological tension, or both. The present study investigates to what extent coronary artery disease explains exhaustion. For this purpose, the relationship between the severity of coronary artery disease and exhaustion, and the relief of exhaustion after successful percutaneous transluminal coronary angioplasty (PTCA) is investigated. Patients who had a successful elective PTCA (N = 120) were evaluated on feelings of exhaustion on admission, 2 weeks after discharge and 6 months after discharge, making use of the Maastricht Questionnaire. Multiple regression analyses were used to investigate to what degree exhaustion on admission and after PTCA was determined by the extent of coronary artery disease and other patient characteristics. Severity of coronary artery disease before PTCA was positively associated with exhaustion and successful PTCA resulted in a significant decrease of exhaustion scores (P < 0.001). However, less than 5% of the variance of the exhaustion scores before PTCA could be explained by severity of coronary artery disease (R2 = 0.04, F = 5.1, P = 0.03). The majority of patients who were exhausted before PTCA remained exhausted after PTCA. Exhaustion was present in 75% of the patients before PTCA and in 65% 2 weeks after PTCA, which indicates that restoration of coronary perfusion by successful PTCA does not substantially reduce the number of exhausted patients. At 6 months, exhaustion was present in 60% of the patients, and there was no difference between patients with and without typical anginal complaints at that time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of successful coronary angioplasty on feelings of exhaustion. 813 36

This report describes an unusual case of secondary nocturnal enuresis presumptively secondary to progressive bradycardia from complete heart block. Congenital complete heart block occurs in approximately 1 of 22,000 livebirths and is typically associated with structural congenital heart disease or maternal collagen vascular diseases. It can be entirely asymptomatic during infancy and childhood, depending in part on the escape rate and rhythm and other hemodynamic variables. The case described above was not diagnosed until the patient coincidentally underwent cardiac monitoring. The picture was confusing initially, as a tricyclic antidepressant medication had been ingested. Heart block is one of the known cardiovascular effects of tricyclic antidepressant overdose. However, the conduction disturbance should have resolved as the drug was excreted from the body. As children with congenital complete heart block get older, the ventricular escape rate typically decreases. In addition, as activity increases with age, more demand is placed for cardiac output. The resting end-diastolic volume is increased to elevate stroke volume in compensation for lower heart rate. As the escape rate decreases and the metabolic demand increases, patients with congenital complete heart block then may begin to develop symptoms. Typical symptoms in children include dizziness, Stokes-Adams syncopal attacks, fatigue, daytime somnolence, and other somatic complaints. Bedwetting has not been reported as an initial symptom, but in this case is likely secondary to the excessive somnolence and difficulty with arousal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nocturnal enuresis secondary to heart block: report of cure by cardiac pacemaker implantation. 833 31

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67

Some patients with pre end-stage congestive heart disease do not receive a significant hemodynamic benefit from dynamic cardiomyoplasty because, during prolonged preoperative immobilization, their latissimus dorsi muscle (LDM) becomes extremely weak. It is the authors' hypothesis that the local administration of an anabolic steroid into an electrically stimulated LDM will produce a thicker and stronger muscle with significant resistance to fatigue. The electrical stimulation training protocol of sheep continued for 8 weeks. For localized anabolic steroid administration an osmotic pump was placed in a subcutaneous pocket and the catheter was introduced into the LDM. The contractile force of electrically stimulated and unstimulated control muscle was studied. Control data were calculated as 100% and all other data were corrected to control. After 4 weeks there was no decrease in contractile force. The change seen was from 88 to 100% with different preloads (10, 15, and 20 g/kg) and amplitudes of impulses (5 and 10 V). After 8 weeks, the LDM was more powerful than before electrical stimulation, with a change of 97-133%. Usually after 8 weeks of electrical stimulation alone, contractile force decreases to 70-75%. During a fatigue test (30 min, 100 bursts per minute, 10-25 Hz, ripple frequency, 10 V impulse amplitude) after 4 and 8 weeks of our protocol, the LDM lost only 12% of its initial force, whereas control muscle lost 40%. Thus local anabolic steroid administration makes the LDM stronger and more useful for cardiomyoplasty.
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PMID:Force enhancement of skeletal muscle used for dynamic cardiomyoplasty and as a skeletal muscle ventricle. 857 55

To clarify the demographic and clinicolaboratory features of postdialysis fatigue (PDF), we enrolled 85 patients on maintenance hemodialysis in a cross-sectional study using validated questionnaires and chart review. Forty-three patients complained of fatigue after dialysis. On formal testing using the Kidney Disease Questionnaire, the PDF group had statistically greater severity of fatigue and somatic complaints than the group of patients without subjective fatigue (P = 0.03 and 0.04, respectively). On a scale measuring intensity of fatigue (1 = least to 5 = worst), the PDF group average was 3.4 +/- 1.2. PDF subjects reported that 80% +/- 25% of dialysis treatments were followed by fatigue symptoms. In 28 (65%) of patients, the symptoms started with the first dialysis treatment. They reported needing an average of 4.8 hours of rest or sleep to overcome the fatigue symptoms (range, 0 to 24 hours). There were no significant differences between patients with and without PDF in the following parameters: age; sex; type of renal disease; presence of diabetes mellitus, heart disease (congestive, ischemic), or chronic obstructive lung disease; blood pressure response to dialysis; type or adequacy of dialysis regimen; hematocrit; electrolytes; blood urea nitrogen; creatinine; cholesterol; albumin; parathyroid hormone; ejection fraction; and use of antihistamines, benzodiazepines, and narcotics. In the fatigue group, there was significantly greater use of antihypertensive medications known to have fatigue as a side effect (P = 0.007). Depression was more common in the fatigue group by Beck Depression score (11.6 +/- 8.0 v 7.8 +/- 6.3; P = 0.02). We conclude that (1) postdialysis fatigue is a common, often incapacitating symptom in patients on chronic extracorporeal dialysis; (2) no routinely measured parameter of clinical or dialytic function appears to predict postdialysis fatigue; and (3) depression is highly associated with postdialysis fatigue, but the cause-effect relationship is unclear.
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PMID:Postdialysis fatigue. 915 12


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