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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Periodic heart rate fluctuation depends on the oscillation of sympathetic and vagal activation of the heart. Periodic retardation and acceleration of heart rate related to respiration and to blood pressure changes can be registered on the ECG as the "variability of R-R intervals". Testing procedures of the variability of R-R intervals at rest, during deep breathing, daily activities, during exercise and other stress tests are described in the paper. For the evaluation of the R-R interval's variability, current statistical methods are used (e.g. mean with standard deviation, variation coefficient, mean beat to beat differences in R-R intervals etc.). Power spectral analysis in the variability of 200-600 successive R-R intervals commonly performed today uses either rapid Fourier transformation or the autoregulation model. The analysis shows high- and low frequency peaks corresponding to the rapid and slow oscillations in heart rate. Evaluation of the R-R interval variability, especially using power spectrum analysis, gave good results in testing drugs, e.g., beta blockers, calcium antagonists and antiarrhythmic drugs. Variability of R-R intervals is reduced in conditions affecting the cardiac autonomous nervous system such as diabetes. It is also decreased in patients with ischaemic heart disease and in those with cardiac failure of different aetiology. The decrease is not an expression of the disease itself: it shows an alteration in neurovegetative tonicity in the particular disease condition. The decreased variability of R-R intervals in patients with ischaemic heart disease has an important prognostic value. The predominance of the sympathetic over the depressed vagal activity signalizes an increased risk of sudden coronary death.
Cor Vasa 1993
PMID:[Variation in the R-R intervals on the electrocardiogram. A new diagnostic method in cardiology]. 844 39

34 patients with ventricular dysfunction (18 in NYHA class II and 16 in NYHA class III heart failure) whose clinical status was stabilized by diuretics and systemic vasodilators, entered a randomized trial to compare the effects of short-term oral digoxin and active placebo on left ventricular diastolic function, non invasively evaluated by echo-Doppler transmitral left ventricular filling flow. At baseline patients were subdivided by reversal--the ratio of peak early (E) and late (A) transmitral filling velocities--E/A < 1 (group I) or normal--E/A > or = 1 (group II) echo-Doppler E/A ratio; group II exhibited a shorter deceleration time (125 +/- 20 ms vs 198 +/- 38 ms, p > 0.05) and isovolumic relaxation time (64 +/- 15 ms vs 93 +/- 10 ms; p < 0.05) as well as a higher peak E velocity (85 +/- 28 cm/s vs 54 +/- 20 cm/s; p < 0.05), ("restrictive" left ventricular filling pattern). After 4 weeks, no changes in all echo-Doppler parameters were noted in group I in response to either oral digoxin or active placebo. Clinical amelioration (defined as reduction by at least one functional class) was observed in 3 patients after digoxin.(ABSTRACT TRUNCATED AT 250 WORDS)
Cor Vasa 1993
PMID:Effects of short-term oral digoxin on left ventricular diastolic filling in patients with ventricular dysfunction. An echo-Doppler study. 850 Feb 97

Left ventricular hypertrophy constitutes an essential risk factor for sudden death, myocardial infarction and heart failure. The death rates of patients with ECG-demonstrated cardiac hypertrophy are 4.8 times as high as those of healthy subjects. Cardiac hypertrophy is associated with a substantially increased incidence of ventricular arrhythmias. The condition is treatable in most patients. While the most effective group of drugs for controlling cardiac hypertrophy are ACE inhibitors; methyldopa, calcium antagonists, and beta-blockers have also proved useful in the management of cardiac hypertrophy in hypertension. Diuretics other than indapamide are not appropriate for treating cardiac hypertrophy. An additional benefit of ACE inhibitor administration is they can favourable affect increased levels of collagen in the hypertrophic myocardium. The prognosis of hypertensive patients, whose treatment has lead to regression in cardiac hypertrophy in hypertension, is markedly better than that of patients in whom regression fails to be achieved. A role in the development of cardiac hypertrophy in hypertension, in addition to the blood pressure level, is played by a number of mechanisms; it is the genetic factor which has received most attention recently. As the prognosis of hypertrophic patients has been found to correlate more closely with left ventricular weight, determined by echocardiography, than with blood pressure, echocardiography should be employed more often in the future to help optimize antihypertensive therapy.
Cor Vasa 1993
PMID:[Cardiac hypertrophy in hypertension--clinical significance and possibilities of control]. 850 Mar

The pathogenesis of preeclampsia stems from aberrant changes at the placental interface. The trophoblastic endovascular invasion of tonic spiral arteries that converts them to passive conduits falters. Uteroplacental insufficiency and fetoplacental hypoxemia result. Secondary maternal oxidative stress and an excessive inflammatory response to pregnancy generate the clinical syndrome of preeclampsia. Current treatment focuses on preventing seizures, controlling hypertension, preserving renal function and delivering the baby. We propose that the pathophysiological changes induced by preeclampsia in the placenta parallel those caused by persistent hypoxemia in the lungs at high altitude or with chronic obstructive pulmonary disease. Unrelenting pulmonary hypoxic vasoconstriction induces pulmonary hypertension and cor pulmonale. Inhalation of nitric oxide and phosphodiesterase-5 inhibitors opposes pulmonary hypoxic vasoconstriction, alleviates pulmonary hypertension and improves systemic oxygenation. Notably nitric oxide donor therapy also counters hypoxemic fetoplacental vasoconstriction, a biological response analogous to pulmonary hypoxic vasoconstriction. Fetal oxygenation and nutrition improve. Placental upstream resistance to umbilical arterial blood flow decreases. Fetal right ventricular impedance falls. Heart failure (cor placentale) is avoided. Emergency preterm delivery can be postponed. Other than low dose aspirin and antioxidants vitamins C and E no available therapy specifically targets the underlying disease profile. We hypothesize that, like nitric oxide donation, pharmacological inhibition of placental phosphodiesterase-5 will also protect the fetus but for a longer time. Biological availability of guanosine 3'5'-cyclic monophosphate is boosted due to slowed hydrolysis. Adenosine 3'5'-cyclic monphosphate levels increase in parallel. Cyclic nucleotide accumulation dilates intact tonic spiral arteries and counters hypoxemic fetoplacental vasoconstriction. Intervillous and intravillous perfusion pick up. Maternal to fetal placental circulatory matching improves. Enhanced placental oxygen uptake alleviates hypoxemic fetal stress. Appropriate fetal nutrition resumes. Cor placentale and severe intrauterine growth restriction are averted. Increased maternal cyclic nucleotide concentrations promote systemic vasodilatation so that blood pressures fall. Preemption of oxidative stress initiated by "consumptive" oxidation of nitric oxide stabilizes the vascular endothelium and corrects coagulopathy. Anti-inflammatory and immunosuppressant adenosine 3'5'-cyclic monphosphate offsets the extreme gestational inflammatory response. Cellular injury and multi-organ damage are prevented. One tablet a day of the new long acting phosphodiesterase-5 inhibitor, tadalafil (half life of 17.5 h) theoretically should allow a preterm pregnancy affected by preeclampsia to continue safely. Selective monitoring of vital organ functions guards against life-threatening maternal complications. Regular biophysical profiling warns the obstetrician of impending fetal compromise. Fetal growth and vital organ maturation can continue. As a result workloads imposed upon neonatal intensivists will lighten. Parental anxiety and concern will be allayed. The cost of treating preeclamptic mothers and their extremely low birth weight infants will decrease. Money saved by midwifery services in poorer states can be used to pay for better prenatal care. Severe preeclampsia/eclampsia will be less common. Maternal and perinatal morbidity and mortality will be reduced. Because the human immunodeficiency virus often infects individuals at a workforce eligible age, the global acquired immunodeficiency syndrome pandemic has already brought many nations to the brink of economic ruin. Potentially productive lives saved for the future will help restore them fiscally.
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PMID:Hypothesis: selective phosphodiesterase-5 inhibition improves outcome in preeclampsia. 1550 76

Cor triatriatum is a congenital malformation of the heart which is usually presented with heart failure. We have dealt with an unusual presentation of a two-month-old child with cor triatriatum presented with hemolytic anemia.
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PMID:Hemolytic anemia: an unusual presentation of cor triatriatum sinistrum. 1962 54

A 20-month old girl with severe pulmonary hypertension and cardiomegaly was admitted to the paediatric intensive care unit with right ventricular failure of unknown origin. Only after decompression of the heart chambers under extracorporeal membrane oxygenation (ECMO), did the pathognomonic membrane of Cor triatriatum become visible on echocardiography. The patient underwent successful surgical correction and subsequently cardiac function recovered completely. Cor triatriatum remains a rare congenital cardiac disorder with a variable presentation, often including recurrent respiratory infections before right-sided heart failure occurs. This case illustrates that ECMO can serve not only as a bridge to diagnosis, but can also facilitate correct diagnosis. Given the excellent outcome after surgical treatment, it is crucial that cardiologists rule out the possibility of cor triatriatum when assessing a child with unexplained pulmonary hypertension.
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PMID:Extracorporeal membrane oxygenation as a bridge to diagnosis in a 20-month old girl with pulmonary hypertension and right ventricular failure. 2296 57

Cor triatriatum is a rare congenital cardiac anomaly accounting for only 0.1-0.4% of all congenital heart diseases usually diagnosed in infancy or childhood and rarely found in adults. It is characterized by fibromuscular membrane dividing the left atrium into two chambers. This congenital heart disease is reported to be frequently associated with variety of cardiac anomalies such as an atrial septal defect, anomalous pulmonary venous drainage, and persistent left superior vena cava. A woman with no cardiac history was admitted to the hospital due to acute heart failure and diagnosed as severe mitral regurgitation and cor triatriatum by pre-orerative transthoracic echocardiography. Emergency mitral valve plasty was undertaken because of the severity of mitral regurgitation without determining the detailed type of cor triatriatum. Thus, diagnosis of the type of cor triatriatum with perioperative transesophageal echocardiography (TEE) was required to establish correct cardiopulmonary bypass and determine the operative procedure. Perioperative TEE revealed that the type was Lucas-Schmidt- I A, and cardiopulmonary bypass was established safely. Operation was performed without any problems. The TEE skill of our anesthesiologists could contribute to the safe management of the cardiac surgery.
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PMID:[Diagnosis and evaluation of a patient with cor triatriatum using perioperative transesophageal echocardiography]. 2472 46

Cor triatriatum sinister (CTS) is a rare congenital abnormality. Clinical presentation of patients with CTS mainly depends on the anatomic features of membrane and may vary from mild or moderate symptoms mimicking mitral stenosis to more severe and complicated cardioembolic stroke or a new onset heart failure. We herein have reported on a young male who presented with the signs and symptoms of mitral stenosis and was diagnosed as CTS with gradient on the orifice of the membrane after transthrocacic echocardiography. Computerized tomographic angiography revealed that the patient had unilateral, left sided pulmonary arterial hypoplasia and pulmonary vein atresia, with only the right pulmonary veins draining into the left atrial chamber. Further cardiac imaging by either computed tomography or magnetic resonance imaging is necessary in order to seek accompanying cardiac and vascular abnormalities. Patients with CTS have improved short and long term survival rates if CTS and accompanying abnormalities are surgically treated before the disease is complicated with heart failure, pulmonary hypertension, stroke and etc.
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PMID:A Very Rare Case of Co-Existence of Cor Triatriatum Sinister and Left Pulmonary Vein Atresia. 2789 67

Cor triatriatum is a rare congenital cardiac anomaly defined by an abnormal septation within the atrium (left or right) leading to inflow obstruction to the respective ventricles. It exists either in isolated classical form or may be associated with simple to complex congenital cardiac anomalies. Several anatomical variants exist even in the classical form, and therefore, it may require multimodal diagnostic modalities to characterize and differentiate for better percutaneous interventional or surgical planning. It commonly presents in infancy but may remain undetected till death. Symptomatology typically mimics mitral and tricuspid stenosis in sinister and dexter varieties, respectively. However, features of systemic embolization, heart failure, atrial fibrillation, cyanosis, cardiac asthma, syncope, and sudden cardiac arrest have also been reported in the literature. Surgical correction under cardiopulmonary bypass is the preferred treatment. Nevertheless, balloon dilatation may be considered in anatomically compatible variants and in special circumstances, such as heart failure, pregnancy, or as a bridge to definitive treatment.
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PMID:Cor Triatriatum: A Review. 2791 70

Cor triatriatum is a rare congenital heart defect that is associated with an increased risk for developing atrial fibrillation. We report a case of a healthy 38-year-old man who presented in decompensated heart failure and atrial fibrillation with a rapid ventricular response. A transthoracic echocardiogram (TTE) demonstrated severe biventricular dysfunction and dilatation in addition to cor triatriatum sinister. He was diuresed with resolution of his symptoms and spontaneously converted back to sinus rhythm. There is limited evidence in the literature surrounding anticoagulation and associated left ventricular dysfunction in the setting of cor triatriatum which posed difficult therapeutic decisions.
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PMID:Cor Triatriatum Sinister: An Unusual Cause of Atrial Fibrillation in Adults. 2980 25


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