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PubMed1995

Government, university, and community collaboration to develop a cardiac surgery database and report of morbidity and mortality while waiting for open heart surgery.

The Provincial Advisory Committee on Cardiovascular Services was established in January of 1990 to advise concerning these services. One of the first tasks assigned was to monitor waiting times for cardiac surgery. Referring cardiologists categorized their patients into four priorities: emergency, urgent-inpatient, urgent-outpatient, and planned. Data of the southern Alberta centers for the past three years were analyzed for events while waiting for surgery. (Median time to event in days) M1=Myocardial Infarction EM=Emergency D=Day A hierarchy was used to assign the single most serious event for patients having more than one event: death>MI>readmission or change from urgent-inpatient to emergency. Events were frequent and unpredictable, particularly in outpatients. Categorization of patient suitable to wait at home for cardiac surgery is imperfect. The risk of having an event while on the waiting list is much greater for out-patients than in-patients: 12.8% (169/1323) versus 1.9% (19/1002). All adverse events for the in-patients occurred at four days--one day less than the proposed maximum waiting time. In the out-patient population, the median waiting time to experiencing adverse events ranged between 32 and 54 days. Target waiting times set by PACCS for these two categories is 14 and 56 days respectively. Total adverse events occurred to 8% of the patients on the waiting list. Median waiting time to experiencing an adverse event while on the list occurs much earlier than suspected: four days in urgent in-patients and 36 days for out-patients; well below the intended maximum of 56 days. This database proved invaluable for this important critical data collection. It is hoped it will serve as a model for similar future projects.

Alberta↗
PubMed1977

[Role of mitral valve dysfunction in the development of cardiac insufficiency in postinfarct cardiosclerosis].

The clinical suggestion on the dysfunction of the mitral valve in 20 patients with post-infarction cardiosclerosis was confirmed by ventriculography (8 persons) and in autopsy (12 persons). The paper presents a clinical characteristics of the both groups of patients, the indices of the central hemodynamics, the end diastolic pressure in the left ventricle of the heart, coronaroangiography, as well as morphometric data of the examination of the hearts and of the extent of the scar lesions of the myocardium in patients who died of congestive cardiac insufficiency against the background of postinfarction cardiosclerosis combined with the papillary muscle affection.

Adult↗
PubMed1998

Pharyngeal colonisation, ADNB response and development of cardiac lesions in mice following intranasal inoculation with group A beta haemolytic streptococcus M type 18.

Swiss albino mice from a randomly bred colony were inoculated intranasally with 1.6, 2 or 2.4 x 10(7) colony forming units of a mid-logarithmic phase culture of group A beta haemolytic streptococcus M type 18 for 3 days, 6 days or once a week respectively for three weeks. Pharyngeal colonisation could be observed in 67 (59.8%) of 112 mice on 4th day after inoculation and 14 (38%) of the 37 mice on 21st day. Out of 27 mice tested for determination of antibodies to deoxyribonuclease B at regular intervals for 98 days, 15 (55.5%) showed responses, with maximum titers varying from 50 units to 4800 units in individual mice. Histopathological evidence for cardiac lesions were seen in five (3.03%) of the 165 animals studied. These included one case of severe endocarditis, two cases of endocarditis with valvular lesions and one case with non-specific lymphocyte infiltration in the heart. One other animal showed subendocardial oval nodular aggregates. Although the cellular nature of these lesions were not determined, this study shows that Swiss albino mice can serve as suitable animal models to study experimental streptococcal infections. However these are preliminary observations and are to be confirmed and revalidated by further controlled experiments.

Animals↗
PubMed1998

[Role and significance of cytokines in the development of cardiac insufficiency].

The hypothesis of immune and inflammatory activation occurring during chronic cardiac failure, capable of maintaining the disease, is supported by many experimental and clinical trials. Plasma cytokines levels, particularly the tumour necrosis factor alpha (TNF alpha), are raised at advanced stages of the disease, especially in cachectic patients. The correlations with other, more traditional markers, especially neurohumoral, are not very close, probably suggesting different mechanisms. Cytokines are a group of very different molecules with multiple, non-specific, and even beneficial effects. However, the lack of regulation in severe cardiac failure may lead to deleterious effects on the heart. The experimental effects of TNF alpha (mini-pumps, transgenic animals) include features of myocarditis, chamber dilatation and contractile dysfunction. Large scale therapeutic trials of long acting TNF alpha antagonists could confirm the "inflammation hypothesis" of mutual interaction between cardiac failure and the production of cytokines.

Cardiac Output, Low↗
PubMed2002

The challenge of pediatric cardiac services in the developing world.

Pediatric cardiac services are too expensive for most developing nations. Problems other than cardiac disease take priority when it comes to budget allocations. Poor health infrastructure and referral systems, malnutrition, and the HIV/AIDS pandemic aggravate the situation, and the increasing economic divide is threatening what services do exist. We highlight how the practice of pediatric cardiac surgery in South Africa compares with first-world standards and outline some of the problems faced by pediatric cardiac services in developing nations.

Cardiac Surgical Procedures↗
PubMed2005

Expression and localization of caveolins during postnatal development in rat heart: implication of thyroid hormone.

Caveolins modulate signaling pathways involved in cardiac development. Caveolin-1 exists in two isoforms: the beta-isoform derivates from an alternative translational start site that creates a protein truncated by 31 amino acids, mainly expressed in endothelial cells, whereas caveolin-3 is present in muscle cells. Our aim was to define caveolin distribution and expression during cardiac postnatal development using immunofluorescence and Western blotting. Caveolin-3 sarcolemmal labeling appeared as dotted lines from days 1 to 5 and as continuous lines after 14 days of age. Caveolin-3 expression, low at birth, increased (4-fold) to reach a maximum (P < 0.05) by day 5 and then decreased to stabilize in adults. Total caveolin-1 and its alpha-isoform were codistributed at birth in endothelial and smooth muscle cells; afterward, only the caveolin-1alpha labeling became limited to endothelium. Quantitative analysis indicated a similar temporal pattern of both total caveolin-1 and caveolin-1alpha expression, suggesting that caveolin-1alpha and -1beta are coregulated; the caveolin-1alpha levels increased fourfold by day 5 to reach a maximum by day 14 (P < 0.05). Tyrosine-14-caveolin-1 phosphorylation, low at birth, increased suddenly around day 14 (8-fold vs. day 1) and returning afterward to basal level. Because the T3/T4 level is maximal by day 14, caveolin-1 expression/phosphorylation profiles were analyzed in hypothyroid heart. The levels of caveolin-1alpha and consequently tyrosine-14-caveolin-1 phosphorylation, but not that of caveolin-3, decreased (50%) in hypothyroid 14-day-old rats. Our data demonstrate that, during postnatal cardiac growth, 1) caveolins are distinctly regulated, and 2) thyroid hormones are involved in caveolin-1alpha expression.

Adaptation, Physiological↗
PubMed1979

Collagen synthesis in the developing chick heart.

We have surveyed the amount and types of collagen synthesized in two regions of the chick heart during embryonic development. Cardiac tissues from successive periods of development were labeled with 3H-proline in short-term organ culture. The fraction of incorporated label present as collagen was estimated by comparison of TCA-soluble radioactivity before and after digestion with purified bacterial collagenase. This measure of collagen synthesis varied only slightly with the length of the labeling period and agreed with values obtained by labeling in ovo. In the developing outflow tract, the fraction of label present as collagen increased sharply during the period of truncal septation (5-9 days), rising from initial values of 6% at 3 days of incubation to a plateau of about 25% (10-19 days). In ventricular myocardium, this fraction rose gradually from 3 to 20% between 3 and 19 days of incubation. The types of collagen synthesized in developing heart were analyzed by limited pepsin digestion and acrylamide gel electrophoresis, using collagens synthesized in tendon, cartilage, skin, and lens capsule for comparison. The types of collagen synthesized in both cardiac regions changed in similar manner during development. During the first week of cardiac function, a substantial but progressively smaller fraction of total collagen synthesized was identified as Type IV. Synthesis of Type I collagen increased sharply during this period and predominated during the second half of development. Type III collagen was synthesized in trace amounts by the middle of development and constituted approximately one-sixth of total collagen synthesis just before hatching. Minor amounts of collagen identified as Type B collagen were synthesized throughout the latter two-thirds of development.

Animals↗
PubMed2003

Development of the cardiac conduction system: a matter of chamber development.

Within one day after the formation of the linear heart an adult type of electrocardiogram (ECG) can be monitored, reflecting the development of coordinated activation of the heart. The possibility that during evolution and ontogenesis of the heat, this development is achieved by localized growth of cardiac chambers rather than of a conduction system is discussed here.

Animals↗
PubMed2001

Cardiac-specific LIM protein FHL2 modifies the hypertrophic response to beta-adrenergic stimulation.

BACKGROUND: A deficiency of muscle LIM protein results in dilated cardiomyopathy, but the function of other LIM proteins in the heart has not been assessed previously. We have characterized the expression and function of FHL2, a heart-specific member of the LIM domain gene family. METHODS AND RESULTS: Expression of FHL2 mRNA and protein was examined by Northern blot, in situ hybridization, and Western blot analyses of fetal and adult mice. FHL2 transcripts are present at embryonic day (E) 7.5 within the cardiac crescent in a pattern that resembles that of Nkx2.5 mRNA. During later stages of cardiac development and in adult animals, FHL2 expression is localized to the myocardium and absent from endocardium, cardiac cushion, outflow tract, or coronary vasculature. The gene encoding FHL2 was disrupted by homologous recombination, and knockout mice devoid of FHL2 were found to undergo normal cardiovascular development. In the absence of FHL2, however, cardiac hypertrophy resulting from chronic infusion of isoproterenol is exaggerated (59% versus 20% increase in heart weight/body weight in FHL null versus wild-type mice; P<0.01). CONCLUSIONS: FHL2 is an early marker of cardiogenic cells and a cardiac-specific LIM protein in the adult. FHL2 is not required for normal cardiac development but modifies the hypertrophic response to beta-adrenergic stimulation.

Adrenergic beta-Agonists↗
PubMed1990

Calcium channel blocker toxicity.

A retrospective review was conducted of all patients who were reported to a regional poison control center after "overdose" of a calcium channel blocker during a two-year period (1987 and 1988). An analysis of 91 patient cases is presented after excluding allergic reactions, cases involving coingestants, and patients lost to follow-up. Patients who developed any symptoms after ingestion were defined as manifesting toxicity. There were 38 cases of verapamil ingestion with toxicity developing in 18 patients. The mean nontoxic dose was 320 mg, whereas the mean toxic ingestion was 3.2 g. Nine patients became hypotensive, 13 developed conduction system abnormalities (sinus node suppression, atrioventricular nodal block, or bundle branch block), and 11 manifested arrhythmias. Ten developed neurological symptoms. There were 31 cases of nifedipine ingestion with toxicity developing in seven patients. The mean nontoxic dose was 19 mg, while the mean toxic ingestion was 340 mg. Four patients were hypotensive, only one developed cardiac conduction abnormalities, and four developed arrhythmias. Three had neurological symptoms. There were 24 cases of diltiazem ingestion with only minor toxicity developing in four patients. There was no statistically significant difference in the frequency of hypotension, arrhythmias, or neurological symptoms in patients who overdosed with verapamil as compared with nifedipine (by Fisher's exact test). However, conduction system abnormalities were more common with verapamil ingestion (P less than .05). Toxic manifestations after diltiazem over-dose were uncommon in our study. Eighteen of the 29 patients who developed toxicity required treatment in excess of gastrointestinal decontamination. Calcium was administered to 14 patients and was helpful in five.

Adolescent↗
PubMed1999

Life-threatening events after theophylline overdose: a 10-year prospective analysis.

BACKGROUND: Despite the declining use of theophylline, episodes of intoxication continue to occur, producing seizures, arrhythmias, and death. OBJECTIVES: To further characterize major toxic effects and to examine the efficacy of existing interventions. METHODS: We conducted a longitudinal cohort study of patients with theophylline overdose. For a 125-month period, all patients referred to the Massachusetts Poison Control System in Boston with a serum theophylline concentration of 167 micromol/L (> or =30 microg/mL) or more were followed up prospectively. Recommended management by the poison center was uniform and protocol based. RESULTS: Three hundred fifty-six patients were enrolled. Mean age was 34.5 years (range, 3 days to 98 years). Mean peak serum theophylline concentration was 336 micromol/L (60 microg/mL) (range, 167-1360 micromol/L [30-245 microg/mL]). One hundred sixty-two patients (45.5%) had acute, 144 (40.4%) had chronic, and 50 (14.0%) had acute-on-therapeutic poisoning. Seventy-four patients (20.8%) developed cardiac arrhythmias, and 29 (8.2%) developed seizures. Fifteen patients (4.2%) died, 11 (73%) of whom had chronic overmedication. Arrhythmias were significantly more common after chronic overmedication than after acute intoxication (35% vs. 10%; odds ratio, 4.97; 95% confidence interval, 2.68-9.23; P<.001). Eight percent of patients with chronic overmedication died compared with 2.5% of those with acute intoxication (odds ratio, 3.20; 95% confidence interval, 1.01-10.39; P = .04). There was no significant difference in the rate of major toxic effects (25.9% vs. 30.0%) or death (4.6% vs. 3.7%) among patients referred from 1986 to 1991 and from 1992 to 1996. CONCLUSIONS: Theophylline intoxication results in substantial morbidity and mortality, particularly in those with chronic overmedication. Treatment strategies fail to improve clinical outcome. With safer alternative options available, the current indications for theophylline should be rigorously evaluated with a goal toward minimal use of this agent.

Acute Disease↗
PubMed2003

Phosphatidylinositol 3-kinase regulates bone morphogenetic protein-2 (BMP-2)-induced myocyte enhancer factor 2A-dependent transcription of BMP-2 gene in cardiomyocyte precursor cells.

The growth and differentiation factor bone morphogenetic protein-2 (BMP-2) regulates cardiac development during vertebrate embryogenesis. In cardiac precursor cells, BMP-2 has recently been shown to induce expression of cardiac transcription factors, including myocyte enhancer factor 2A (MEF-2A). The specific signal transduction mechanism by which BMP-2 regulates these actions is not known. We investigated the role of phosphatidylinositol (PI) 3-kinase in regulating these processes in cardiomyocyte precursor CL6 cells. BMP-2 increased PI 3-kinase activity in these cells in a time-dependent manner, resulting in increased expression of sarcomeric myosin heavy chain (MHC) and MEF-2A. Inhibition of PI 3-kinase abolished these actions of BMP-2, indicating the involvement of PI 3-kinase in these processes. Furthermore, BMP-2 stimulated specific protein.DNA complex formation when an MEF-2 DNA recognition element was used as probe. Antibody supershift assay confirmed the presence of MEF-2A in this protein.DNA complex. Inhibition of PI 3-kinase activity completely prevented the MEF-2A.DNA complex formation. BMP-2 also increased transcription of a reporter gene driven by an MEF-2-specific DNA element in a PI 3-kinase-dependent manner. Ectopic expression of MEF-2A increased BMP-2 transcription to the same extent induced by BMP-2, indicating that MEF-2A may participate in BMP-2 autoregulation in CL6 cells. Expression of dominant negative PI 3-kinase completely abolished BMP-2-induced as well as MEF-2A-mediated BMP-2 transcription. Furthermore expression of MEF-2A increased MHC expression in a PI 3-kinase-dependent manner. Together these data provide the first evidence that BMP-2-induced PI 3-kinase signaling regulates MEF-2A expression and define a mechanism of MEF-2A-dependent BMP-2 transcription.

Adenoviridae↗