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PubMed1994

Female infant with oncocytic cardiomyopathy and microphthalmia with linear skin defects (MLS): a clue to the pathogenesis of oncocytic cardiomyopathy?

A infant girl had red stellate skin lesions on the cheeks and neck, and mildly short palpebral fissures. Her skin abnormality was typical of microphthalmia with linear skin defects (MLS), a newly recognized syndrome consisting of congenital linear skin defects and ocular abnormalities in females monosomic for Xp22. She died suddenly and unexpectedly at age 4 months; the cause of death was ascribed to oncocytic cardiomyopathy. Oncocytic cardiomyopathy occurs only in young children, who present with refractory arrhythmias leading to cardiac arrest. The coexistence of two rare conditions, one of which is mapped to the X chromosome, and an excess of affected females with oncocytic cardiomyopathy, make it likely that oncocytic cardiomyopathy is also X-linked, with Xp22 being a candidate region. Overlapping manifestations in the two conditions (ocular abnormalities in cases of oncocytic cardiomyopathy and arrhythmias in MLS) offer additional support for this hypothesis.

Abnormalities, Multiple↗
PubMed1999

Pulmonary venous flow in hypertrophic cardiomyopathy as assessed by the transoesophageal approach. The additive value of pulmonary venous flow and left atrial size variables in estimating the mitral inflow pattern in hypertrophic cardiomyopathy.

AIMS: This study was conducted to assess the characteristics of the pattern of pulmonary venous flow and to document the interaction of this flow and left atrial function with the pattern of mitral inflow in hypertrophic cardiomyopathy. METHODS AND RESULTS: Pulmonary venous and mitral flows were evaluated by the transoesophageal approach in 80 patients with hypertrophic cardiomyopathy. Left atrial size and function were measured by the transthoracic approach. Their values were compared with those obtained from 35 normal controls. Twelve patients showed significant (> 2+) mitral regurgitation. As a group, hypertrophic cardiomyopathy patients showed increased atrial reversal flow and longer deceleration time of the diastolic wave, but a wide variability of pulmonary venous flow patterns were observed. Thirty patients (37.5%) had pseudonormal mitral flow patterns. Stepwise multilinear regression analysis identified the ratio of systolic to diastolic pulmonary venous flow velocity, the ratio of velocity-time integrals of both flow waves at atrial contraction, the left atrial minimal volume and the systolic fraction as independent predictive variables of the mitral E/A wave velocity ratio (r = 0.82). By logistic regression, the former three variables were selected as independent predictive covariates of a pseudonormal mitral flow pattern (sensitivity: 83%, specificity: 90%). The ratio of velocity-time integrals of both atrial waves was the most important predictive variable in both analyses. CONCLUSIONS: The observed variability in the configuration of pulmonary venous flow velocity waveform is related to what occurs in transmitral flow in patients with hypertrophic cardiomyopathy. Significant mitral regurgitation is not an independent correlate of pseudonormal mitral inflow patterns in these patients. Our results further emphasize the complementary, additive value of the pulmonary venous flow velocity pattern and left atrial size in the interpretation of the mitral flow velocity pattern, and indirectly suggest the underlying increased left ventricular filling pressures of patients with hypertrophic cardiomyopathy and pseudonormal mitral flow patterns.

Adult↗
PubMed1993

Pathophysiological and biochemical characterisation of an avian model of dilated cardiomyopathy: comparison to findings in human dilated cardiomyopathy.

OBJECTIVE: With the recent availability of human myocardium, many animal models have been shown to be unsuitable as models of human heart failure. The aim of this study was to describe the pathophysiological changes in a model of dilated cardiomyopathy in turkey poults and to compare them to results obtained from failing human hearts. METHODS: After receiving furazolidone for 2-3 weeks, animals developed cardiomyopathy (Fz-DCM) and were studied at the whole heart and isolated muscle level. Myofibrillar ATPase activity and noradrenaline turnover were determined in tissue homogenates in failing and non-failing control hearts. RESULTS: Fz-DCM animals had greater heart weights, heart weight/body weight ratios, and end diastolic volumes. Fractional shortening of the left ventricle and systolic blood pressures were reduced (p < 0.01) in myopathic animals. Isolated perfused hearts had lower peak developed pressures (p < 0.01). Isolated muscle preparations showed no significant differences in peak twitch forces between control and Fz-DCM muscles at a 1 Hz stimulation rate. The relationship between force and frequency of stimulation was positive in control muscles up to 1.7 Hz, whereas in Fz-DCM muscles the relationship was sharply negative above 1 Hz. Time to 80% relaxation was markedly slower in the Fz-DCM muscles. Although [Ca2+]o responsiveness was similar for Fz-DCM and normal animals, responsiveness to isoprenaline was significantly reduced in Fz-DCM hearts. Cardiomyopathic animals displayed diminished noradrenaline content in the left ventricle. Fractional noradrenaline turnover was higher (p < 0.05) in the cardiomyopathic birds. In skinned fibre preparations from control and Fz-DCM hearts calcium activations were similar. Maximum myofibrillar ATPase activities were, however, significantly lower in myopathic animals and myofibrillar protein content was reduced by 25%. CONCLUSIONS: In this model of dilated cardiomyopathy: (1) relaxation is markedly prolonged; (2) the response to beta adrenergic stimulation is diminished; (3) Mg-ATPase activities and myofibrillar protein content are reduced; and (4) sympathetic activity in the heart is markedly increased with depletion of noradrenaline stores. Furthermore, a reduction in tissue noradrenaline content per se is a misleading index of the dynamic state of cardiac noradrenaline stores. With its similarities to human cardiomyopathy, this model promises to provide new insights into the pathophysiology and progression of dilated cardiomyopathy.

Adenosine Triphosphatases↗
PubMed1995

Myocardial calcium-independent nitric oxide synthase activity is present in dilated cardiomyopathy, myocarditis, and postpartum cardiomyopathy but not in ischaemic or valvar heart disease.

OBJECTIVE: To determine the activity of the calcium-dependent constitutive (cNOS) and calcium-independent inducible nitric oxide (iNOS) synthases in heart tissue from patients with different cardiac diseases. PATIENTS AND DESIGN: Endomyocardial biopsy specimens were obtained from patients with dilated hearts (by echocardiography and ventriculography) and normal coronary arteries (by selective angiography). Recognised clinical, radiological, and histopathological criteria were used to diagnose non-inflammatory dilated cardiomyopathy (DCM) (n = 6), inflammatory cardiomyopathy (ICM) (n = 5), and peripartum cardiomyopathy (PPCM) (n = 3). Comparative groups were chosen with similarly dilated hearts caused by ischaemic (n = 5) or valvar disease (n = 4), and, in addition, non-dilated hearts with ischaemic (n = 5) and valvar (n = 3) disease. Venous blood was taken at the time of myocardial biopsy for assay of plasma tumour necrosis factor alpha (TNF alpha). RESULTS: Myocardial tissue from patients with DCM, ICM, and PPCM showed considerable iNOS activity (16.8 (2.7) pmol citrulline/mg protein/min) with little or no cNOS activity (1.3 (0.9) pmol citrulline/mg protein/min). In contrast, myocardial tissue from patients with both dilated and non-dilated hearts of ischaemic or valvar aetiology showed cNOS and little, if any, iNOS activity (dilated--cNOS 11.7 (2.4) and iNOS 0.8 (0.6) pmol citrulline/mg protein/min; non-dilated--cNOS 12.1 (1.8) and iNOS 1.4 (0.8) pmol citrulline/mg protein/min). Plasma TNF alpha was detectable only in patients with inflammatory DCM. CONCLUSIONS: These results support the hypothesis the generation of nitric oxide by iNOS accounts for some of the dilatation and impaired contractility associated with inflammatory and non-inflammatory dilated cardiomyopathy and peripartum cardiomyopathy.

Adult↗
PubMed1986

Peripartum maternal cardiomyopathy with idiopathic cardiomyopathy in the offspring. A case report.

Peripartum cardiomyopathy is an enigmatic disorder. A patient who developed it after delivery had a twin pregnancy complicated by demise of one fetus, preterm labor and subsequent preterm delivery of the viable twin, who died at 48 hours of life. The second twin had autopsy evidence of idiopathic cardiomyopathy, as did a prior child, who had died at 2 years of age. This report is the first on a woman with peripartum cardiomyopathy associated with idiopathic cardiomyopathy in her live-born infant. Our findings, in conjunction with those noted in a review of the literature, suggest that there is a subset of peripartum cardiomyopathy that may be mediated on a genetic or immunologic basis.

Adult↗
PubMed1993

Autonomic nervous system activity in idiopathic dilated cardiomyopathy and in hypertrophic cardiomyopathy.

To assess autonomic nervous activity in patients with cardiomyopathies, analysis of heart rate variability was performed using 24-hour ambulatory electrocardiograms in 14 patients with idiopathic dilated cardiomyopathy (IDC), 15 with hypertrophic cardiomyopathy (HC) and 18 healthy subjects. Heart rate variability during the night and daytime was calculated using fast-Fourier transform, and power spectra were quantified in 2 frequency bandwidths: 0.00 to 0.15 Hz (low-frequency power [LF]) and 0.15 to 0.50 Hz (high-frequency power [HF]). Log(HF) was used as an index of parasympathetic nervous activity, and log(LF/HF), of sympathetic nervous activity. Log(HF) was significantly lower and log(LF/HF) was significantly higher in IDC. These changes were related to ejection fraction. In HC, lower log(HF) and higher log(LF/HF) were recognized only during the night, and these changes were independent of the degree of myocardial hypertrophy. Our results indicated attenuation of parasympathetic activity and enhanced sympathetic activity in HC during the night, and also in IDC. Assessment of autonomic imbalance by analysis of heart rate variability may be useful for understanding the pathophysiology of cardiomyopathies.

Autonomic Nervous System↗
PubMedDate not supplied

Are failured cardiomyopathies a zinc-deficit related disease? A study on Zn and Cu in patients with chronic failured dilated and hypertrophic cardiomyopathies.

BACKGROUND: Muscle zinc deficit may be important in cardiac failure pathogenesis. We studied whether Zn deficit is present in dilated (DCM) and hypertrophic (HCM) cardiomyopathies with chronic cardiac failure. The aim was to find out whether it might be a diagnostic and prognostic marker. METHODS: Zn and Cu values were measured in plasma, urine and red blood cells by flame atomic absorption spectrophotometer in normal subjects, in 15 patients with DCM and in 11 patients with HCM in chronic cardiac failure. RESULTS: There is a statistically important increase of zincuria as well as low plasmatic and erythrocytic zinc in DCM; low plasmatic and erythrocytic zinc was found in HCM. CONCLUSIONS: It is likely that chronic cardiac failure, by atrial natriuretic peptide activation, increases zincuria and involves a secondary loss of plasmatic and erythrocytic zinc. Primitive or secondary zinc deficit causes marked structural and functional myocardial cell impairment. Hypozinchemia from increased zincuria seems to represent an important diagnostic and prognostic marker in chronic failured cardiomyopathies. Dilated cardiomyopathy, particularly in elder subjects, may be considered as a primitive or a secondary Zn-deficit myocardial disease. In the essay, the possible pathogenetic mechanisms underlying hypozinchemia and determining functional and structural myocardial cell changes are discussed. The main consequence of present results is pharmacological Zn administration as a new pathogenetic therapy in chronic failured cardiomyopathies.

Aged↗
PubMed2000

[Epidemiology of dilated cardiomyopathy and hypertrophic cardiomyopathy].

Epidemiological study in Akita City revealed that the Japanese prevalence of dilated cardiomyopathy was 12.5 per 100,000 population at the end of 1994, and the mean age of patients with dilated cardiomyopathy was 63 +/- 12 years. The prevalence was comparable with that of 9.03 per 100,000 population in Niigata Prefecture and with that of 15 per 100,000 population by the echocardiographic mass screening in 2,673 subjects from 12 Japanese rural areas. The prevalence of hypertrophic cardiomyopathy in Japan was 170 to 574 per 100,000 population by mass screening. In future, the genetic analysis may compensate the limitation of morphological diagnosis of cardiomyopathies and also reveal new aspects of these disorders.

Aged↗
PubMed1991

Myocardial accumulation of monoclonal antimyosin Fab in hypertrophic cardiomyopathy and postpartum cardiomyopathy.

Indium-111-antimyosin Fab scan was performed in patients with hypertrophic and postpartum cardiomyopathies to assess whether or not myocardial damage can be delineated. In two patients with hypertrophic cardiomyopathy, intense and diffuse antimyosin uptake was observed, although there was no evidence of acute myocardial damage or wall motion abnormality. A patient with postpartum cardiomyopathy showed a dense and relatively localized accumulation in the left ventricular anterior wall in association with thallium perfusion and wall motion abnormalities. Thus, antimyosin scanning can delineate not only manifested but also subclinical myocardial damage in hypertrophic and postpartum cardiomyopathies which may not be detectable by other techniques.

Adult↗
PubMed1995

[Identical male twins showing progression from hypertrophic cardiomyopathy to dilated cardiomyopathy-like features].

Twenty-three-year-old identical male twins with hypertrophic cardiomyopathy which progressed into the dilated phase are reported. The younger brothers first presented at age 16 with an abnormal electrocardiogram. Hypertrophic nonobstructive cardiomyopathy with an asymmetric septal hypertrophy was diagnosed. He was treated with beta-blocker, but he stopped taking the drug as he had no symptoms at that time. He presented again at age 21 years with symptoms of apparent congestive heart failure. Echocardiography showed marked dilatation of the left ventricle with thin wall which was compatible with dilated cardiomyopathy. The elder brother presented with an initial echocardiogram showing systolic anterior movement of the mitral valve without asymmetric septal hypertrophy. He presented again with his brother aged 21 years when his echocardiogram showed slight dilatation of the left ventricle, although he did not complain of cardiac symptoms. These identical twins are the first reported cases of hypertrophic cardiomyopathy progressing to the deteriorated dilated phase.

Adult↗
PubMed1996

Mapping the locus for familial hypertrophic cardiomyopathy to chromosome 11 in a family with a case of apical hypertrophic cardiomyopathy of the Japanese type.

To identify the disease locus of familial hypertrophic cardiomyopathy (FHC) in a Chinese family, a genetic linkage study was performed using polymorphisms from various chromosomal regions. This family has eight affected members, including a case with typical features of apical hypertrophic cardiomyopathy of the Japanese type. The results revealed significant evidence of linkage of polymorphisms on chromosome 11p13-q13 and FHC in this family with a maximal lod score of 3.38 at theta = 0.00. Our data suggest that the locus responsible for FHC in this family maps to chromosome 11 and that the molecular basis of FHC in the case of apical hypertrophic cardiomyopathy of the Japanese type might be similar to that of other affected members in the same family. Further studies are needed to elucidate the whole spectrum of the genetic basis of apical hypertrophic cardiomyopathy of the Japanese type.

Base Sequence↗
PubMed1982

Hypertrophic cardiomyopathy with ventricular septal hypertrophy localized to the apical region of the left ventricle (apical hypertrophic cardiomyopathy).

Clinical and morphologic features are described in a unique subgroup of seven patients with hypertrophic cardiomyopathy. Five patients either died suddenly or are alive but severely symptomatic. In each patient ventricular septal hypertrophy was demonstrated on two dimensional echocardiography or at necropsy to be virtually confined to its apical one-half. However, conventional M mode echocardiography was unreliable in identifying this site of hypertrophy because it was often inaccessible to the path of the M mode beam. Apical distribution of septal hypertrophy does not constitute a separate disease entity, but rather appears to be part of the morphologic spectrum of hypertrophic cardiomyopathy, as judged from two findings: (1) genetic transmission of hypertrophic cardiomyopathy in relatives of each study patient; and (2) marked disorganization of cardiac muscle cells in the left ventricular wall of the two patients studied at necropsy. Apical distribution of septal hypertrophy in these patients was associated with relatively mild T wave inversion in the electrocardiogram and characteristic angiographic appearance of the left ventricle with mid ventricular constriction and a small, often poorly contractile apical segment. These electrocardiographic and angiographic features differ from those previously described in Japanese patients with "apical hypertrophic cardiomyopathy" in whom "giant" T wave inversion and a "spade-like" appearance of the left ventricle were characteristic.

Adolescent↗
PubMed1990

Naturally occurring cardiomyopathy in the Doberman pinscher: a possible large animal model of human cardiomyopathy?

Currently there is no large animal model of dilated cardiomyopathy. The smaller animal models of cardiomyopathy, such as the Syrian hamster, cannot be studied with echocardiography and cardiac catheterization, and the relevance of these models to human dilated cardiomyopathy is open to question. On the basis of some initial observations in Doberman pinschers, it was speculated that these dogs could have occult left ventricular dysfunction. Accordingly, studies were performed in 46 apparently healthy Doberman pinschers and in 41 mongrel dogs: two-dimensional echocardiography (30 dogs in each group), cardiac catheterization (16 Doberman pinschers and 12 mongrels) and coronary blood flow studies (13 Doberman pinschers and 6 mongrels). In the awake, unsedated dogs studied with echocardiography, left ventricular wall thickening was significantly less in the Dobermans than in the mongrels (28% versus 36%, p = 0.0003). In the anesthetized dogs undergoing cardiac catheterization, left ventricular ejection fraction was significantly lower in the Dobermans than in the mongrels (0.38 versus 0.63, p = 0.0001). Rest coronary blood flow and coronary blood flow reserve were similar in the two groups. It is concluded that apparently healthy Doberman pinschers have occult left ventricular dysfunction. These dogs may serve as a large animal model of dilated cardiomyopathy and should not be used experimentally to study normal cardiac physiology.

Animals↗
PubMed2005

Evaluation of left bundle branch block as a reversible cause of non-ischaemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy.

OBJECTIVES: We sought to determine if amelioration of left bundle branch block (LBBB)-induced contraction disturbances achieved by left ventricular (LV)-based pacing could result in sustained reversal of severe LV dysfunction in certain patients with chronic heart failure due to non-ischaemic cardiomyopathy. BACKGROUND: It has been shown that LBBB induces asynchronous contraction of LV. However, whether such a functional contraction disturbance, if present for an extended period of time, could account for a dilated cardiomyopathy remains unknown. METHODS: The study population comprised 29 patients with dilated cardiomyopathy, sinus rhythm, LBBB and severe heart failure (14 patients in New York Heart Association (NYHA) class III and 15 in class IV). Patients were followed prospectively after resynchronization therapy. LV function was considered to be normalized when ejection fraction (EF) was >50% at 1 year. RESULTS: Five among the 29 patients (17%: group 1) demonstrated both complete normalization of LV function following resynchronization therapy (EF: from 19+/-6 to 55+/-3%, P = 0.001) and clinical improvement (mean NYHA class: 3.4+/-0.5 to 1.8+/-0.4, P = 0.02; 6-min walk distance: 300+/-136 to 444+/-75 m, P = 0.12; peak VO2: 11.9+/-4 to 15.8+/-2 ml/min/kg, p = 0.03). Among the remaining 24 patients (83%: group 2) EF improved but did not normalize (from 21+/-8 to 23+/-11%, ns). Baseline clinical features could not predict which patients would exhibit the reversal of LV dysfunction. CONCLUSIONS: Normalization of LV function 1 year after resynchronization therapy in a small but important number of patients suggests that long-standing LBBB may be a newly identified reversible cause of cardiomyopathy.

Aged↗
PubMed2005

Transient mid-ventricular ballooning cardiomyopathy: a new entity of Takotsubo cardiomyopathy.

We present a case of a 64-year-old man with transient mid-ventricular ballooning cardiomyopathy. Left ventriculography showed morphological differences with ballooning around the whole mid-portion of the left ventricle, although precipitating factors and clinical courses were similar to Takotsubo cardiomyopathy. We suspect that transient mid-ventricular ballooning cardiomyopathy is a new pathological entity in Takotsubo cardiomyopathy.

Cardiomyopathies↗
PubMed1995

Dipyridamole echocardiography for diagnosis of coexistent coronary artery disease in hypertrophic cardiomyopathy. Echo-Persantine International Cooperative (EPIC) Study Group--Subproject Hypertrophic Cardiomyopathy.

The recognition of coexistent coronary artery disease (CAD) in patients with hypertrophic cardiomyopathy may be difficult by noninvasive testing based upon electrocardiographic changes or perfusion defects. Dipyridamole-stress echocardiography has proved a sensitive and highly specific test for noninvasive diagnosis of CAD in various patient subsets. To establish the feasibility, safety, and diagnostic accuracy of dipyridamole-stress echocardiography in patients with hypertrophic cardiomyopathy, we performed high-dose dipyridamole testing (up to 0.84 mg/kg over 10 minutes) in 88 patients with hypertrophic cardiomyopathy (63 men; mean age +/- SD, 46 +/- 17 years). A subset of 60 patients was referred for coronary angiography independently of test results; CAD was defined as > or = 50% diameter narrowing in at least 1 major coronary vessel. Dipyridamole echocardiography/electrocardiography testing was completed in all patients, with no limiting side effects or adverse reactions. In the subgroup of 60 patients with coronary angiography (14 with and 46 without CAD), chest pain occurred in 18 patients (8 with and 10 without CAD, p = NS); ST-segment depression > or = 2 mm from baseline in 28 (7 with and 21 without CAD, p = NS); and transient dyssynergy in 10 patients (10 with and none without CAD, p < 0.0001). Assuming the transient regional dyssynergy to be the only criterion of positivity, the dipyridamole echocardiography test showed 71% sensitivity, 100% specificity, 100% positive predictive value, and 93% diagnostic accuracy for diagnosis of angiographically assessed CAD. We conclude that high-dose dipyridamole echocardiography testing may be considered a feasible and accurate tool for the noninvasive diagnosis of CAD in patients with hypertrophic cardiomyopathy.

Adult↗
PubMed1999

Significant improvement of quality of life following atrioventricular synchronous pacing in patients with hypertrophic obstructive cardiomyopathy. Data from 1 year of follow-up. PIC study group. Pacing In Cardiomyopathy.

AIMS: Atrioventricular synchronous pacing exerts beneficial effects, including reduction of left ventricular outflow tract gradients, in patients with hypertrophic obstructive cardiomyopathy. The Pacing in Cardiomyopathy study was initiated to explore the effects of pacing in a double-blind randomized crossover fashion. The aims were to ascertain the beneficial effects of pacing in a controlled study and to rule out a placebo effect by pacing. This paper deals with the outcome of pacing on quality of life during 1 year of follow-up. METHODS: Quality of life was evaluated with the Karolinska questionnaire, validated for patients paced for bradyarrhythmias and ischaemic heart disease. Drug-refractory patients with hypertrophic obstructive cardiomyopathy were recruited for the study and after a temporary pacing procedure implanted with permanent pacemakers. Patients were randomized to two study arms defining the sequence of pacemaker programming. In one arm the pacemaker was inactive, in the other active. After 3 months the pacemaker was reprogrammed to the alternate mode and a further 3 months followed. After this period subsequent pacemaker programming corresponded to the mode preferred by the patient. A last assessment was made 1 year after baseline examinations. RESULTS: Eighty patients completed the first crossover period and 75 completed the full 1 year of follow-up. Active pacing induced significant quality of life improvements, in the order of 9-44%, regardless of programming sequence. Discontinuation of pacing after a first active period resulted in the return of symptoms. Fourteen patients requested early reprogramming after having been programmed to inactive pacing after a first period of active pacing. Seventy-six patients preferred active pacing after the crossover period. A further 6 months of pacing induced progressive improvement in symptoms already favourably influenced. CONCLUSION: Atrioventricular synchronous pacing has a profound beneficial effect on most domains of quality of life in patients with hypertrophic obstructive cardiomyopathy refractory to drug treatment.

Adult↗
PubMed1995

Respiratory illness, beta-agonists, and risk of idiopathic dilated cardiomyopathy. The Washington, DC, Dilated Cardiomyopathy Study.

An epidemiologic study was carried out to examine the possible role of beta-agonists and other respiratory medications in the development of idiopathic dilated cardiomyopathy. Associations with respiratory medications, bronchial asthma, emphysema, and chronic bronchitis were examined by comparing newly diagnosed cases (n = 129) ascertained from five Washington, DC, area hospitals for the period 1990-1992 with neighborhood controls (n = 258) identified by using a random digit dialing technique. The cases and controls were matched on sex and 5-year age intervals and were compared in the analysis using conditional logistic regression methods. A statistically significant association was observed between idiopathic dilated cardiomyopathy and history of emphysema or chronic bronchitis (adjusted odds ratio (OR) = 4.4, 95% confidence interval (CI) 1.6-12.4). The association with bronchial asthma was of borderline significance (adjusted OR = 1.9, 95% CI 0.9-4.2). Associations were also observed with use of oral beta-agonists (adjusted OR = 3.4, 95% CI 1.1-11.0) and beta-agonist inhalers or nebulization (adjusted OR = 3.2, 95% CI 1.4-7.1), as well as with use of oral corticosteroids, inhaled corticosteroids or cromolyn, and theophylline medications. A total of 20.0% (23 of 115) of the cases had a reported history of beta-agonist inhaler use compared with 6.7% (17 of 254) of the controls. The strength of these associations was diminished when the temporal relation between exposure to beta-agonist inhalers or oral preparations and clinical diagnosis of idiopathic dilated cardiomyopathy was taken into account, however, and the associations with duration of beta-agonist medication use were not statistically significant (p > 0.05). The results of this study suggest, but do not prove, that use of beta-agonists has an etiologic role in idiopathic dilated cardiomyopathy.

Adrenergic beta-Agonists↗