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PubMed1980

Lung biopsy specimens in the evaluation of pulmonary vascular disease.

Open lung biopsy specimens in 72 patients were submitted for evaluation of pulmonary vascular disease. In nine instances, the specimens were inadequate for this purpose. Essentially, there were three indications for taking a lung biopsy specimen. The first was unexplained pulmonary hypertension with 40 patients in this category; plexogenic pulmonary arteriopathy was diagnosed in 14, and chronic pulmonary thromboembolism in 12. Others included pulmonary venoocclusive disease in two patients; two other patients had pulmonary vascular lesions in their lung biopsy specimens, indicative of chronic hypoxic pulmonary hypertension; and ten patients had severe arterial as well as venous alterations that could have been caused by obstruction to pulmonary venous flow as well as by fibrosis of lung tissue. Since we realized this possible source of error, we have submitted these two alternative possibilities to the clinician. In a heterogeneous group of eight patients, the nature of acquired or congenital heart disease remained doubtful in spite of extensive clinical investigation. In several instances, the biopsy specimen contributed to establishing the diagnosis of the cardiac condition. Finally, in a group of 15 patients with known congenital cardiac disease and pulmonary hypertension, whose state of pulmonary vasculature was considered borderline as far as the possibility of corrective surgery of the cardiac defect was concerned, lung biopsy specimens helped to determine the feasibility of surgery. The results show that in a restricted group of patients with pulmonary vascular disease, a biopsy of the lung has a place in establishing the nature and severity of the vascular alterations.

Adolescent↗
PubMed2006

Influenza- and RSV-associated hospitalizations among adults.

We estimated influenza- and respiratory syncytial virus (RSV)-associated hospitalizations by age, high-risk status and outcome, during the 1996/1997-1999/2000 respiratory seasons among adults who did not receive influenza vaccine. Using three health maintenance organization (HMO) databases and local viral surveillance data, we identified weeks when influenza and RSV were circulating and estimated influenza- and RSV-associated hospitalizations. Persons aged > or = 65 years with and without high-risk conditions had significantly increased rates of influenza-associated hospitalizations for pneumonia and influenza, and circulatory and respiratory diseases. Persons aged > or = 65 years with high-risk conditions also had significantly increased rates of influenza-associated hospitalizations for cardiac conditions (16.9 per 10,000 person periods). Relative to the influenza estimates for high-risk persons > or = 65 years, we found lower rates of RSV-associated hospitalizations for pneumonia and influenza diseases (23.4 per 10,000 person periods), cardiac diseases (4.3 per 10,000 person periods) and circulatory and respiratory diseases (44.0 per 10,000 person periods). Among low-risk persons aged 50-64 years, we did not identify significantly elevated rates of influenza- or RSV-associated hospitalizations. Excess hospitalization estimates among adults aged > or = 65 years and high-risk 50-64 year olds during the influenza season suggest that these groups should have priority for influenza vaccine during vaccine shortages.

Adolescent↗
PubMed2002

[Significance of nitric oxide function in development of cardiac hypertrophy under condition of experimental renal hypertension].

The development of cardiac hypertrophy was studied under condition of experimental renal hypertension on the rat. The number of cardiac nitric oxide synthase (NOS)-positive neurones increased simultaneously with the increase in NOS-activity in these neurones. A connection was found between the development of cardiac hypertrophy and the activity of NOS in cardiomiocytes. The involvement of NO in the development cardiac hypertrophy as auto- and paracrine regulator is supposed.

Animals↗
PubMed2001

Measurement of myocardial beta-adrenoceptor density in clinical studies: a role for positron emission tomography?

The beta-adrenoceptor (beta-AR) plays an important role in the regulation of heart function and has been extensively studied in recent decades. In vitro studies have shown down-regulation of beta-AR density in heart failure and cardiac conditions that may lead to heart failure. As in vitro measurements on cardiac tissue samples do not allow longitudinal and regional assessment of myocardial beta-ARs in humans, new methods are being developed to measure beta-ARs in vivo using positron emission tomography (PET). Studies using PET and the radioligand [(11)C]CGP 12177 have shown promising results that are in agreement with those of in vitro studies. However, the radiochemical synthesis of [(11)C]CGP 12177 is very demanding, preventing its widespread use. Hence, new radioligands are being developed using simpler methods of radiochemical synthesis. ( S)-[(11)C]CGP 12388 has been presented as a promising new radioligand. So far, in vivo measurements of beta-AR density using PET have mainly been performed to confirm in vitro studies. Using the full potential of PET, performance of regional measurements and longitudinal studies might add further knowledge on the pathophysiological role of the beta-AR in cardiac disease and the effect of interventions. Furthermore, PET might gain a role in the clinical management of patients with abnormalities of cardiac contractile function.

Carbon Radioisotopes↗
PubMed2004

Successful lysis of intra-cardiac thrombi with streptokinase in patients with renal failure; two case reports and review of the literature.

In situ formation of thrombi within the cardiac cavities carries a substantial risk of morbidity and mortality due to the inherent danger of embolization to vital organs. This typically occurs in patients with underlying cardiac disorders associated with low flow state favoring regional stagnation of blood and subsequent clotting. Occasionally, extra-cardiac conditions such as renal failure predispose to the development of intra-cardiac thrombi in the presence or absence of identifiable cardiac abnormalities. Once identified, the appropriate treatment of such thrombi remains highly controversial. Here, we report on the successful and safe use of streptokinase in two patients with end stage renal disease with high risk left ventricular, right ventricular and right atrial thrombi.

Adult↗
PubMed1997

Cardiac rehabilitation services in England and Wales: a national survey.

We sent a short postal questionnaire to 244 centres in England and Wales that admitted patients with cardiac conditions. In total, 199 (81%) of the centres claimed to provide a cardiac rehabilitation service. Of these, 25 were randomly selected as a representative sample and visited in order to obtain detailed information concerning the provision of services. Most (18 (72%)) of the centres had commenced their rehabilitation programme within the previous 5 years, usually at the instigation of interested staff. Patient entry to cardiac rehabilitation programmes was restricted; women (who represented only 15% of attenders), elderly people (excluded in 10 (40%) centres), and those with more complex problems, such as angina or heart failure, were under-represented. The central components of all programmes were education and exercise training but there was a wide range in the quantity and quality of service provision. Most (22 (88%)) programmes were hospital out-patient based, one (4%) was hospital in-patient based, one (4%) was community-based and one (4%) was home-based. The staffing and funding of programmes was variable, with 7 (28%) having no identified funding. There are wide variations in the resources currently available for the rehabilitation of patients with coronary heart disease. There is a need for clearer direction of these services, in particular to determine minimum service provision. Guidelines are necessary to give a framework for this relatively new and rapidly expanding service.

Aged↗
PubMed2000

Cardioprotective effects of MET-88, a gamma-butyrobetaine hydroxylase inhibitor, on cardiac dysfunction induced by ischemia/reperfusion in isolated rat hearts.

Inhibition of fatty acid metabolite accumulation may be beneficial for treatment of cardiac dysfunction induced by ischemia. MET-88, 3-(2,2,2-trimethylhydrazinium)propionate dihydrate, inhibits gamma-butyrobetaine hydroxylase which catalyzes conversion of gamma-butyrobetaine to carnitine. In this study, we investigated whether MET-88 has cardioprotective effects against cardiac dysfunction induced by ischemia/reperfusion. Rats were divided into four groups: (1) control; (2) MET-88 at 50 mg/kg; (3) MET-88 at 100 mg/kg; (4) nifedipine at 30 mg/kg. MET-88 was administered orally once a day for 10 days, and nifedipine was administered orally 30 min before the experiments. Cardiac functions (heart rate, left ventricular systolic pressure and coronary flow) were measured in rat working heart preparations for 30 min under ischemia followed by 20 min under reperfusion. Myocardial carnitine levels were measured at the end of the experiments. Before ischemia, MET-88 did not affect cardiac functions, but nifedipine significantly increased only coronary flow. Under the ischemic condition, cardiac functions were markedly decreased in all groups. During reperfusion, MET-88 and nifedipine promoted recovery of cardiac functions and decreased the incidence of ventricular fibrillation. MET-88 also prevented the accumulation of long-chain acylcarnitine induced by ischemia. These results indicated that MET-88 protected against cardiac dysfunction in ischemia/reperfusion, and preventing the accumulation of long-chain acylcarnitine may be responsible for the cardioprotective effects.

Animals↗
PubMed1992

A corrected transposition of the great arteries with situs inversus visceralis and cleft palate, but without other cardiac defects.

A 17-year-old female admitted for cleft palate surgery was referred for further evaluation of her cardiac condition. The patient had been diagnosed as dextrocardia at birth, without any cardiac murmurs. She has led a normal life. The apical impulse was felt at the fifth intercostal space at the right mid-clavicular line. The ECG and chest x-rays were strongly suggestive of corrected transposition of the great arteries (CTGA) with situs inversus visceralis. Findings of the two-dimensional and Dopplar echocardiograms showed CTGA with a mild morphologic tricuspid regurgitation without any other complicated cardiac anomalies. In the Japanese literature, 36 CTGA patients without associated cardiac defects have been reported. Of these, four patients revealed dextrocardia. To our knowledge, our patient is the first reported adult case without any cardiac defects, only minimal tricuspid regurgitation, situs inversus totalis and cleft palate.

Abnormalities, Multiple↗
PubMed2006

[Neonatal hypocalcaemic dilated myocardiopathy due to a 22q11 microdeletion].

Here we report 2 cases of hypocalcemic cardiomyopathy revealing a 22q11 microdeletion syndrome. This presentation at diagnosis is rare as the cardiac phenotype is mainly made of conotruncal congenital heart defects in this condition. Cardiac failure was diagnosed during the neonatal period in the 2 cases and was associated with profound hypocalcemia. As usual, treatment with calcium and vitamin D led to the regression of the hypocalcemia and the left ventricular function was fully restored. While this circumstances are unusual, we recommend that screening for 22q11 deletion should be performed when confronted to hypocalcemic cardiomyopathy or left ventricular systolic dysfunction in conotruncal defects in neonates.

Calcium↗
PubMed1991

[Fetal echocardiography].

Fetal echocardiography is an ultrasonic technique for the diagnosis of cardiac defects and fetal arrhythmias. During 1981-1990 we examined 1800 women referred for elective examinations from all over the country. Most, at high risk for fetal cardiac anomalies, were examined in the 22nd week of gestation. Others were examined whenever a fetal arrhythmia or a cardiac defect was suspected. In 251 fetuses (13.9%) pathological cardiac conditions were found, and structural heart defects in 51 (2.8%). When a cardiac defect with poor prognosis was diagnosed during the 2nd trimester, termination of pregnancy was suggested. In 35% of these cases termination of pregnancy was accepted. In 12% of the women examined spontaneous intra-uterine fetal death had occurred, while in 52% live babies were born, but half died within 6 months. In 215 fetuses (11.9%) a cardiac arrhythmia was found, which in 73% consisted of supraventricular premature beats. In 15.8% the fetus was endangered by the arrhythmia, mainly supraventricular tachycardia, atrial fibrillation or atrial flutter. Treatment was by drugs administered to the mother. In 1 case of complete A-V block echocardiographic follow-up demonstrated rapid deterioration of heart function. Delivery was induced and a pacemaker was implanted in the newborn.

Arrhythmias, Cardiac↗
PubMed1997

Exertional chest pain in an intercollegiate athlete.

OBJECTIVE: To present the case of an intercollegiate soccer player who collapsed twice within a week during vigorous exercise, with radiating chest pain and dyspnea. BACKGROUND: Episodes of chest pain or syncope in athletes are often alarming and may signal an underlying cardiac condition. Recognition and management of these athletes is vital to the reduction of sudden cardiac death in athletics. DIFFERENTIAL DIAGNOSIS: Cardiac arrest, structural abnormality, valvular dysfunction, coronary artery disease, anomalous coronary artery, coronary vasospasm, asthma. TREATMENT: Standard treatment in these cases requires stabilization of the athlete and identification of the cause of chest pain. An electrocardiogram, echocardiogram, and exercise electrocardiogram demonstrated asymmetric T-wave inversion but otherwise were within normal limits. After the second episode of collapse, the athlete underwent extensive noninvasive cardiopulmonary testing. The athlete did not consent to cardiac catheterization; an angiogram was not obtained. UNIQUENESS: A diagnosis of chest pain, unknown etiology, was offered. The athlete was permitted to return to athletics with this clinical diagnosis. No condition was identified as the cause of the chest pain or abnormal ECG. CONCLUSIONS: Further testing may have identified the cause of chest pain, but the athlete did not consent to this. Recent research indicates that some signs and symptoms previously considered benign may serve as indicators for sudden death candidates.

Journal Article↗
PubMed2005

Etiopathogenesis of arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterised by progressive fibro-fatty replacement of right ventricular myocardium. Earlier studies described ARVC as non-inflammatory, non-coronary disorder associated with arrhythmias, heart failure and sudden death due to functional exclusion of the right ventricle. Molecular genetic studies have identified nine different loci associated with ARVC; accordingly each locus is implicated for each type of ARVC (ARVC1-ARVC9). So far five genes have been identified as containing pathogenic mutations for ARVC. Though mutations in each of the gene/s indicate disruption of different pathways leading to the condition, the exact pathogenesis of the condition is still obscure. This review tries to understand the pathogenesis of the condition by examining the individual proteins implicated and relate them to the pathways that could play a role in the aetiology of the condition. Cardiac ryanodine receptor (RYR-2), which regulates intra-cellular Ca(2+) concentration by releasing Ca(2+) reserves from the sarcoplasmic reticulum (SR), was the first gene for ARVC. The mutation in this gene is believed to disrupt coupled gating of RYR-2, causing after-depolarisation, leading to arrhythmias followed by structural changes due to altered intra-cellular Ca(2+) levels. Three other genes implicated for ARVC, plakoglobin (Naxos disease), desmoplakin (ARVC8) and plakophilin (ARVC9) have prompted the speculation that ARVC is primarily a disease of desmosomes. But identification of TGFbeta-3 for ARVC1 and the role of all these three genes (plakoglobin, desmoplakin and plakophilin) in cardiac morphogenesis indicate some kind of signal-transducing pathway disruption in the condition. The finding that ARVC as a milder form of Uhl's anomaly indicates similar ontogeny for the condition. Further, discovery of apoptotic cells in the autopsy of the right ventricular myocardium of ARVC patients does indicate a common pathway for different types of ARVCs, which is more specific for the right ventricular myocardium involving desmosomal plaque proteins, growth factors and Ca(2+) receptors.

Arrhythmogenic Right Ventricular Dysplasia↗
PubMed2004

Physical conditioning modulates rat cardiac vascular endothelial growth factor gene expression in nitric oxide-deficient hypertension.

Many individuals with cardiac diseases undergo periodic physical conditioning with or without medication to improve cardiovascular health. Therefore, this study investigated the interaction of physical training and chronic nitric oxide synthase (NOS) inhibitor (nitro-L-arginine methyl ester, L-NAME) treatment on blood pressure (BP), cardiac vascular endothelial factor (VEGF) gene expression, and nitric oxide (NO) systems in rats. Fisher 344 rats were divided into four groups and treated as follows: (1) sedentary control, (2) exercise training (ET) for 8 weeks, (3) L-NAME (10mg/kg, s.c. for 8 weeks), and (4) ET+L-NAME. BP was monitored with tail-cuff method. The animals were sacrificed 24h after last treatments and hearts were isolated and analyzed. Physical conditioning significantly increased respiratory exchange ratio, cardiac NO levels, NOS activity, endothelial eNOS, and inducible iNOS protein expression as well as VEGF gene expression. Training also caused depletion of cardiac malondialdehyde (MDA) levels indicating the beneficial effects of the training. Chronic L-NAME administration resulted in a depletion of cardiac NO level, NOS activity, and eNOS, nNOS, and iNOS protein expressions, as well as VEGF gene expression (2-fold increase in VEGF mRNA). Chronic L-NAME administration also enhanced cardiac MDA levels indicating cardiac oxidative injury. These biochemical changes were accompanied by increases in BP after L-NAME administration. Interaction of training and NOS inhibitor treatment resulted in normalization of BP and up-regulation of cardiac VEGF gene expression. The data suggest that physical conditioning attenuated the oxidative injury caused by chronic NOS inhibition by up-regulating the cardiac VEGF and NO levels and lowering the BP in rats.

Animals↗
PubMed1992

Factors enhancing cardiac output in resting subjects during cold exposure in air environment.

Six young males, in semi-nude conditions, resting in dorsal reclining position, were exposed successively to a thermoneutral environment (30 min), a cold environment (1 degree C) (Cold) or thermoneutrality (Control) (120 min), and during 60 min recovery in thermoneutral conditions. Cardiac output has been measured using a Dual Beam Doppler. During cold stress a significant increase of heart rate (66.4 +/- 6.4 to 91.0 +/- 14.9 beats.min-1), systolic blood pressure (119.5 +/- 7.8 to 218.7 +/- 18.7 mmHg), diastolic blood pressure (68.1 +/- 11.7 to 114.3 +/- 28.3 mmHg) and cardiac output (5.42 +/- 0.96 to 8.08 +/- 1.28 l.min-1) were observed. On the contrary initial systolic aorta flow acceleration is significantly lowered (1130 +/- 120 to 840 +/- 170 cm.s-2). Systolic ejection volume remained unchanged throughout the whole experiment. Increase in cardiac output during cold air (1 degree C) exposure is thus only imputed to the higher heart rate partly due to hypersecretion of catecholamines. The diminution of the blood flow acceleration could be related to a lesser arterial compliance and/or to the cold induced hemoconcentration. Enhanced heart's mechanical work due to sympathetic stimulation, seems thus to be absorbed by the increase in the peripheral resistance.

Adult↗
PubMed1978

Conditioning under carbolonium bromide and D--tubocurarine chloride paralysis.

The findings of past research using d-tubocurarine chloride as a control procedure in heart rate conditioning have been equivocal. The present experiment compared classical heart rate conditioning under neuromuscular blockade by d-tubocurarine chloride, and a pharmacologically more specific blocker, carbolonium bromide. Both groups were compared to a placebo condition. The results indicated that carbolonium bromide and placebo treated animals acquired deceleratory cardiac conditional responses, but animals treated with d-tubocurarine chloride did not. Unconditional acceleratory responses were found in groups. The findings were discussed in relation to classical conditioning and the psychopharmacology of neuromuscular blockade.

Animals↗
PubMed2004

[Pregnancy and the heart].

Pregnancy causes important alterations in the cardiovascular haemodynamics which have important bearing in the case of pre-existing cardiac disease. In addition, cardiovascular medications may be contraindicated in pregnant women. With a better recognition of the specific interactions between pregnancy and cardiac conditions, it is now possible to allow pregnancies in numerous women with recognised cardiac diseases.

Cardiovascular Agents↗
PubMed1994

Intracellular acidification and ADP enhance nicorandil induction of ATP sensitive potassium channel current in cardiomyocytes.

OBJECTIVE: Potassium channel openers target ATP sensitive potassium (KATP) channels, and might be beneficial in the treatment of ischaemic cardiac conditions. Ischaemia is associated with an increase in the concentrations of intracellular nucleoside diphosphates and protons, two regulators of KATP channels. Since it is largely unknown whether these factors modulate the action of potassium channel openers, the aim of this study was to define the effects of ADP and intracellular acidification on KATP channel activation by nicorandil, a potassium channel opener currently in clinical use. METHODS: To measure ionic currents, the whole cell patch clamp technique was employed in guinea pig single ventricular myocytes. Induction of KATP channel current by pinacidil, a potassium channel opener chemically unrelated to nicorandil, was used for comparison. RESULTS: Nicorandil (300 microM) and pinacidil (100 microM) induced a time independent K+ current, which was inhibited by glibenclamide (6 microM), a selective blocker of KATP channels. ADP in the pipette solution was required for the nicorandil induced activation of KATP channels when the pH of the pipette solution was 7.2. In the absence of ADP, lowering the pH of the pipette solution to 6.5 was necessary for nicorandil to induce KATP channel current. For pinacidil to induce KATP channel current neither the addition of intracellular ADP nor acidification was required. CONCLUSIONS: Nicorandil may activate KATP channel current more effectively in conditions associated with a change in intracellular proton and ADP concentrations such as cardiac ischaemia.

Action Potentials↗
PubMed1992

Counseling adolescents with congenital heart disease.

Adolescents with congenital heart disease need information regarding their cardiac condition and health care needs, including any life-style implications of the cardiac diagnosis. Pertinent topics to be addressed include preventive health care needs, physical activity (recreational and vocational considerations), pregnancy and contraception issues, and psychosocial stresses of adolescents. Sensitive counseling and health education by nurses can promote the physical health and psychosocial adaptation of adolescents with congenital heart disease.

Adaptation, Psychological↗