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)

Normal adaptation to extra-uterine life consists of an immediate increase in endothelial and smooth muscle cell (SMC) surface: volume ratio as the cells 'spread' in the vessel wall. Lumen diameter increases and resistance falls. Changes in SMC shape are associated with a transient depolymerization of contractile and cytoskeletal filaments. The four SMC phenotypes identified in the vessel wall rapidly show postnatal changes in the types of filament proteins and contractile-associated proteins, indicating that the term 'differentiation' means little at this age. At birth, all SMCs have a predominantly synthetic phenotype. Endothelium-dependent relaxation is relatively poor despite abundant nitric oxide synthase. SMCs are relatively insensitive to nitric oxide despite a high basal generation and a stimulated increase in cGMP generation. By contrast, the relaxation in response to ATP-sensitive potassium (KATP) channel activation is present at birth, the response being similar to that seen in the adult. Neonatal pulmonary hypertension, due to either congenital heart disease or experimental chronic hypobaric hypoxia (51 kPa) is associated with abnormal structural remodelling. In experimental pulmonary hypertension, the normal maturation of endothelium-dependent and -independent relaxation via soluble guanylate cyclase is delayed in newborns and the established responses are inhibited in older animals. The relaxant response to KATP channel activation is preserved. Thus, adaptation to extra-uterine life consists of a rapid sequence of integrated morphological and functional changes, which is disturbed by the presence of pulmonary hypertension. The pattern of recovery from a pulmonary hypertensive insult is determined by the age at exposure and type and duration of the insult.
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PMID:Development of the normal and hypertensive pulmonary vasculature. 854 73

To achieve satisfactory mitral valve repair, we applied continuous warm blood cardioplegia to seven children with congenital heart disease associated with mitral valve insufficiency. All patients had mild to moderate mitral valve regurgitation before the operation. The competency of the mitral valve was assessed by injecting test solution into the left ventricle through the mitral valve orifice with the heart beating under warm blood perfusion into the aortic root proximal to the cross-clamp. Repair of the mitral valve was performed under normothermic cardiac arrest with continuous antegrade perfusion of warm blood cardioplegia. In all patients, these two procedures could be alternated with ease and safety simply by varying the potassium concentration of cardioplegia. While satisfactory valve repair was obtained with the initial procedure in 4 cases, repair was repeated twice in two and three times in one. There were no operative deaths and no complications directly related to the procedure. Postoperative echocardiography demonstrated good mitral valve function with none to trivial regurgitation in six patients (86%). Continuous warm blood cardioplegia is a useful and safe tool for mitral valve repair.
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PMID:Mitral valve repair using continuous warm blood cardioplegia. 871 Apr

Data were analyzed on 290 children admitted consecutively to the pediatric intensive care unit (PICU) of the Postgraduate Institute of Medical Education and Research in Chandigarh, India, in 1993 to examine the frequency, severity, risk factors, and mortality of hypokalemia (3.5 mEq/l serum potassium) and the efficacy of treatment. 43 (14.8%) children had 54 episodes of hypokalemia. Most (68.6%) episodes were moderate. Predisposing factors were the nature of primary disease (renal disease 19%, septicemia 19%, acute diarrhea 14%, and heart disease with congestive failure and meningoencephalitis 12% each), malnutrition (weight for age 80% in 72%), and treatment with drugs (diuretics 20%, beta-agonists 13%, and corticosteroids 11%). Diagnoses most common in hypokalemia cases were acute renal failure (25%), septicemia (22.8%), and acute severe bronchial asthma (20%). The most important predisposing factor for hypokalemia prior to hospitalization was poor oral intake (i.e., inability to replace adequate potassium) (27%). All 43 children received 4-6 mEq potassium/100 ml of intravenous fluids. Clinicians administered an infusion of 0.3 mEq potassium/kg/hour to 7 children (9 episodes) who had ECG changes of hypokalemia until the ECG became normal. Potassium levels returned to normal in all 9 episodes requiring rapid correction and in 40 of 45 episodes requiring slow correction. PICU patients with hypokalemia were more likely to die than PICU patients with no hypokalemia (25.6% vs. 10.9%; p 0.05; odds ratio = 2.34). Hypokalemia patients who received slow correction therapy were more likely to die than those who received rapid correction therapy (31% vs 0; p 0.05). Mortality was lower in PICU patients whose hypokalemia was corrected than in PICU patients whose hypokalemia was not corrected (13.5% vs. 100%; p 0.05). Based on these findings, regular monitoring and rapid correction are recommended to improve the outcome of hypokalemia.
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PMID:Hypokalemia in a pediatric intensive care unit. 877 44

MORTALITY FROM MYOCARDIAL INFARCTION: Primary prevention of coronary heart disease in hypertension is important because the mortality among those who have suffered a myocardial infarction is around 50% within 1 month of the infarction. Although the mortality of those who reach hospital has about halved over the last decade (to about 8%), prevention is the only way to affect coronary mortality overall. OVERALL PREVENTION OF CORONARY HEART DISEASE: There are several proven strategies, involving both drugs and lifestyle changes. Stopping smoking is the most powerful, but exercise and reduction of dietary fats and salt are also important; the latter will need co-operation with the food industry. TREATING HYPERTENSIVES WITH A CORONARY RISK: Lipid-lowering drugs will be needed for some, but not all hypertensives, depending on the coronary risk. Some drug treatments which lower blood pressure (e.g. short-acting formulations of nifedipine) may not reduce the coronary risk; further data or newer preparations are awaited. Potassium-sparing diuretics (particularly in elderly patients) and/or beta-blockers remain the first choice for primary prevention. If a calcium channel blocker is needed, verapamil or diltiazem are useful in patients with no left ventricular dysfunction.
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PMID:Primary prevention of coronary heart disease in hypertension. 893 76

Mature cardiomyocytes have been shown to possess a cyclic AMP-mediated chloride channel (I(Cl)) which is the product of the cystic fibrosis transmembrane regulator (CFTR) gene. Species variability has been demonstrated for other ion channels. This study was designed to evaluate human I(Cl) regulation using the whole-cell patch-clamp bioassay. Atrial tissue obtained from children undergoing congenital heart surgery was enzymatically dispersed into isolated myocytes. The patients ranged in age from 1 day to 11 years (mean 2 years). Isoproterenol was used to activate the cAMP second-messenger system in a potassium-free environment. Membrane calcium and sodium channels were pharmacologically blocked. Of 20 human atrial myocytes obtained from 13 pediatric patients, 80% had a small basal chloride current. The current could be inhibited by the anion transport blocker, 9-anthracene carboxylic acid. In 4 of 20 otherwise viable myocytes, no I(Cl) could be elicited, either at baseline or with beta-adrenergic stimulation. Of the 16 myocytes with a basal I(Cl), the current was unaffected by cAMP stimulation in 15 (94%) cells. There were no significant differences in age, gender or clinical status of patients whose cells conducted Cl- current compared with patients whose myocytes had no measurable I(Cl). Ten mature guinea pig ventricular myocytes were evaluated using the same whole-cell patch-clamp technique. Seven of 10 cells showed a reversible increase in I(Cl) with isoproterenol exposure. Despite presence of the CFTR gene in human cardiomyocytes, functional expression of the cAMP-activated I(Cl) does not appear evident in isolated pediatric atrial myocytes. Whether the pathophysiology of congenital heart disease may influence chloride current modulation via alterations in adrenergic tone, intracellular Ca2+ regulation, and cellular osmotic conditions remains to be established.
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PMID:Lack of cystic fibrosis transmembrane regulator-type chloride current in pediatric human atrial myocytes. 900 Jun 43

Inward rectifying potassium currents (Ikr and Iks) during phase 3 repolarization of the myocyte from the beginning to the end of repolarization of the myocardial syncytium will inscribe a T-U-wave on the surface electrocardiogram (ECG). Type two congenital long QT syndrome (LQT2) is a phenotype of human ether-a-go-go-related gene (HERG) mutation on the chromosome 7q 35-36. Type one congenital long QT syndrome (LQT1) is a phenotype of KvLQT1 mutation on the chromosome 11p15.5. Both LQT1 and LQT2 relate with inward rectifying potassium currents and is repolarization related, therefore, it is speculate that patients of LQT1 and LQT2 may have an abnormal T-U-wave on their surface ECG. To two probands of congenital LQT, 8 patients of structural heart disease treated by open heart surgery, 13 patients of structural heart disease without open-heart surgery, and 10 patients of normal controls, 24 hour-Holter monitoring was performed from July to December 1996. Their corrected QT interval (QTc) as well as the RR interval of every heart beat was calculated by a computer. The results showed that all 33 patients exhibited beat-by-beat fluctuation of their QTc and RR daily. The RR intervals of these two probands of congenital LQT were somewhile more than 1200 ms during circadian waking time, while 31 cases without LQT showed their RR prolongation only during the circadian sleeping time. A multi-undulant T-U-wave, or a beat-to-beat changing of vectors or amplitudes of their T-U-wave observed in these two probands of congenital LQT, were not observable in those 31 patients without congenital LQT. Therefore, we concluded that multi-undulant T-U-wave, sinus bradycardia and a longer QTc was a phenotype of the mutated genes which control the inward rectifying potassium currents during phase 3 repolarization.
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PMID:Multi-undulant T-U-wave, sinus bradycardia and long QT syndrome: a possible phenotype of mutant genes controlling the inward potassium rectifiers. 929 27

The beneficial effects of a stable prostacyclin analogue (PGI2-A), OP 41483 against myocardial ischemic injury were experimentally and clinically evaluated. In 31P-NMR study, the preischemic treatment with PGI2-A prevented myocardial ATP depletion of rat hearts which were subjected to 20 min global ischemia. In patients with congenital heart disease, the PGI2-A of 300 ng/ml was added to the glucose-insulin-potassium cardioplegia (PGI2-group), and this group was compared to control group without PGI2-A in terms of postoperative maximal leakage of CPK-MB (maxCPK-MB). In patients under 1 yr or patients over 1 yr with aortic cross clamp time exceeded 120 min, the maxCPK-MB was significantly (p < 0.05) reduced as compared to the control. This stable PGI2 analogue has shown significant myocardial protective effects experimentally and also in clinical setting.
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PMID:[Experimental and clinical assessment of myocardial protective effect of a prostacyclin analogue (OP 41483)]. 930 17

During recent years there has been an increasing but still controversial discussion on the antiarrhythmic effects and overall benefit of magnesium when directed to patients with various types of ventricular tachyarrhythmias. While magnesium is considered to be a simple, safe and cost-effective approach and many casuistic and empiric reports have indicated antiarrhythmic properties of magnesium in patients with suspected or manifest ventricular arrhythmias, controlled studies proving the antiarrhythmic and overall benefit and justifying a broader use of magnesium in treating various types of ventricular arrhythmias are missing or rare. At present, antiarrhythmic properties and clinical benefit of magnesium application has only been established in patients with torsade de pointes and digitalis-induced ventricular tachyarrhythmias. In perioperative patients at risk for ventricular tachyarrhythmias and in patients suffering from manifest heart failure, data may also indicate some antiarrhythmic properties of magnesium, however, in this case with a wide consensus that the prevention of magnesium deficit is more effective and preferred in most patients over the therapeutic application of magnesium. Another group of patients who may profit from such a therapeutic approach are patients with frequent ventricular arrhythmias and stable underlying heart disease, in whom a recently published double-blind, randomized study documented an antiarrhythmic effect of a 3 week treatment with potassium and magnesium. For all other types of ventricular tachyarrhythmias, the therapeutic use of magnesium can be considered as not harmful, but also as not proven to be effective.
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PMID:[Magnesium deficiency and magnesium substitution. Effect on ventricular cardiac arrhythmias of various etiology]. 933 93

Consuming a diet rich in plant foods will provide a milieu of phytochemicals, nonnutritive substances in plants that possess health-protective benefits. Nuts, whole grains, fruits, and vegetables contain an abundance of phenolic compounds, terpenoids, pigments, and other natural antioxidants that have been associated with protection from and/or treatment of chronic disease such as heart disease, cancer, diabetes, and hypertension as well as other medical conditions. The foods and herbs with the highest anticancer activity include garlic, soybeans, cabbage, ginger, licorice, and the umbelliferous vegetables. Citrus, in addition to providing an ample supply of vitamin C, folic acid, potassium, and pectin, contains a host of active phytochemicals. The phytochemicals in grains reduce the risk of cardiovascular disease and cancer.
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PMID:Phytochemicals: guardians of our health. 933 91

Azimilide, a novel class III antiarrhythmic agent, blocks both the slowly activating (IKs) and rapidly activating (IKr) components of the delayed rectifier potassium current, which distinguishes it from conventional potassium channel blockers such as sotalol and dofetilide, which block only IKr. Azimilide is being developed to prolong the time to recurrence of atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia in patients with and without structural heart disease. Azimilide is also being studied for its role in prevention of sudden cardiac death in high-risk patients after myocardial infarction (MI). Preclinical and clinical studies indicate that azimilide prolongs cardiac refractory period in a dose-dependent manner, as manifested by increases in action potential duration, QTc interval, and effective refractory period. Azimilide does not affect PR or QRS interval and minimally affects hemodynamic properties such as blood pressure and heart rate. Its in vivo effects appear to be rate-independent and are maintained under ischemic or hypoxic conditions, properties of potential clinical significance. Azimilide has shown excellent efficacy (>85%) in suppressing supraventricular arrhythmias in a variety of dog models. It also suppressed complex ventricular arrhythmias in infarcted dogs and, in a sudden death cardiac model, decreased mortality. Azimilide pharmacokinetics are very predictable. The drug is completely absorbed, and the extent of absorption is not affected by food. It can be administered once daily. Clinical data suggest that dose adjustments of azimilide are not required for age, gender, hepatic or renal function, or concomitant use of digoxin or warfarin. Azimilide has a good safety profile in open-label safety studies in >800 supraventricular arrhythmia patients, most with structural heart disease. The incidence of serious adverse events, including torsade de pointes, is low. The rate of patient withdrawal from long-term studies is also encouragingly low. Unlike amiodarone, azimilide has shown no evidence of pulmonary or ocular toxicity. Azimilide is expected to provide a unique new therapy for the prevention of supraventricular arrhythmias and sudden cardiac death when Phase III clinical trials are complete and safety and efficacy are confirmed.
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PMID:Azimilide dihydrochloride, a novel antiarrhythmic agent. 953 22


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