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Seventy-eight men with borderline hypertension according to the World Health Organization criteria underwent echocardiographic examination, followed by simultaneous ambulatory blood pressure and electrocardiographic monitorings for 24 h. The prevalence of echocardiographic left ventricular hypertrophy was 16.6% (13/78). Borderline hypertensives with left ventricular hypertrophy had more supraventricular (P less than .001) and ventricular ectopic beats (P less than .001) than normotensive controls and borderline hypertensives without cardiac involvement. Furthermore, ventricular ectopic activity was significantly related to left ventricular mass (r = 0.58, P less than .05) in borderline hypertensives showing echocardiographic evidence of left ventricular hypertrophy. Our findings suggest that noninvasive assessment of target organ status, including echocardiography, should be employed to optimize risk stratification in borderline hypertension.

The anatomic incidence of left ventricular false tendons has been determined in 100 hearts obtained from consecutive autopsies on patients who had a wide variety of cardiac conditions. In this series, an anomalous band was found in 34 cases. A retrospective two-dimensional (2D) echocardiographic study was able to identify false tendons in only 18 percent of cases with anatomic evidence of them, indicating 2 mm as the limit of resolution of 2D echocardiography even with appropriate projections. Finally, the histologic examination has shown false tendons to contain conduction tissue and thus it is assumed to be intracavitary radiations of the bundle of His. This last consideration introduces new physical and electrophysiologic implications. (Chest 1990; 98:129-32)

We thank Drs Maron and Basso for their comments. The intention of the authors was not to report in their article an additional epidemiological study on hypertrophic cardiomyopathy (HCM) nor to describe a new entity, but an attempt to investigate the possible causes of abrupt disease destabilization, particularly in the context …

Percutaneous transvenous biopsy of an isolated obstructing mass of superior vena cava (SVC) is reported. Basilic vein access and King's endomyocardial bioptome have been successfully used. Metastatic cancer of SVC has been diagnosed and radiochemotherapy instituted, avoiding an undesirable thoracotomy.

A 15 year old girl with a history of asthma had, at the age of 9 years, a diagnosis of idiopathic dilated cardiomyopathy (IDCM). On admission the patient was asymptomatic, with no medical treatment. Peripheral blood eosinophilia was absent. Resting ECG revealed a sinus rhythm with a left bundle branch block. Two …

1991;99;262-263 Chest A Frustaci, M Caldarulo, V di Rienzo, M A Russo and N Gentiloni Antiarrhythmic effect of H-2 antihistamines. http://chestjournal.chestpubs.org/content/99/1/262.citation can be found online on the World Wide Web at: The online version of this article, along with updated information and services ) ISSN:0012-3692 http://chestjournal.chestpubs.org/site/misc/reprints.xhtml ( without the prior written permission of the copyright holder. reserved. No part of this article or PDF may be reproduced or distributed Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights of been published monthly since 1935. Copyright1991by the American College is the official journal of the American College of Chest Physicians. It has Chest

Seventeen young patients (10 males and 7 females, aged 14 to 38 years, mean 26.4) without overt organic heart disease, who had been resuscitated from sudden cardiac arrest and referred to our institution during the period 1984 to 1993 for diagnostic evaluation and electrophysiologic study-guided antiarrhythmic therapy, were studied. Patients underwent noninvasive (electrocardiography, echocardiography [2-dimensional and Doppler], and magnetic resonance imaging) and invasive (left ventricular [LV], right ventricular [RV], and coronary angiography, ergonovine testing, electrophysiologic study, and biventricular endomyocardial biopsy) cardiac studies. Six to 8 biopsy fragments per patient were processed for histology and electron microscopy and read by a pathologist blinded to clinical data. Antiarrhythmic drug testing included amiodarone, propafenone, and metoprolol. A cardioverter-defibrillator was implanted in patients with persistently inducible sustained ventricular tachycardia or ventricular fibrillation. Sequential cardiac biopsy specimens were obtained in patients with active myocarditis undergoing immunosuppressive treatment. Periodic 3-month follow-ups included echocardiography and Holter monitoring. Two groups of patients were distinguished by invasive and noninvasive examinations: group I consisted of 9 patients with entirely normal parameters; group II consisted of 8 patients with structural, nonspecific cardiac abnormalities. In this latter group, mild to moderate dilatation and hypokinesia of the left ventricle were documented in 4 patients, concentric LV hypertrophy was seen in three patients, and RV dysfunction was noted in 1 patient. Histologic examination was abnormal in in all patients and revealed specific lesions in 65% of them; LV biopsy specimens allowed a diagnosis in 3 of 7 myocarditic patients with normal RV histology.(ABSTRACT TRUNCATED AT 250 WORDS)

Summary A case of severe hypokalaemia with stupor, skeletal muscle and heart muscle damage is reported. An initial infusion of glucose-insulin and potassium (GIK) produced a temporary clinical improvement with reduction of creatine kinase (CKMB) and elevation of serum K+. On the 4th day of treatment, neuromuscular and cardiovascular deterioration occurred accompanied by a further rise of CKMB. This deterioration was coincident with a serum phosphate of 0.26 mmol/l. The impaired left ventricular (LV) function was measured using echocardiography and detecting the ejection fraction (EF). GIK was stopped and a potassium phosphate infusion commenced. As the phosphate and potassium deficiencies were corrected, the neuromuscular and cardiac abnormalities resolved, CKMB fell to normal and LVEF rose from 40% to 72%. We suggest that additional cardiac damage due to hypophosphataemia may have occurred in this patient, who already had cardiac impairment as a result of profound hypokalaemia. Possible mechanisms are discussed.

A case of ankylosing spondylitis with aortic valve disease and hearing loss is described. A series of radiographic and audiometric investigations showed the hearing loss to be of a conductive type. It seemed most likely that the hearing loss was related to an inflammatory involvement of the ossicular joints due to the primary disease. No other case of conductive hearing loss has previously been reported due to otoarthritis in ankylosing spondylitis. This is important both theoretically and practically.

Congestive heart failure developed in a patient with low electrocardiographic QRS voltages, diffuse thickening of the septum and free cardiac wall, and a reduction in left ventricular internal diameter, which suggested an infiltrative heart muscle disease. Histological examination at necropsy showed hypertrophic cardiomyopathy with symmetrical left ventricular hypertrophy. Myocardial disarray of type 1A disorganisation was extensive and equally distributed in the ventricular septum and the left anterior and left posterior ventricular free walls. Severe fibrosis (40%) was also present and may have been a possible cause of the electrocardiographic abnormalities as well as of the lack of ventricular dilatation.

Dilated cardiomyopathy and right ventricular dysplasia, although their aetiologies are unknown, are separate entities which can be recognized by endomyocardial biopsy (EMB) and differentiated from other heart muscle diseases. Biventricular EMB is the most appropriate approach for the diagnosis. Histological definition is relevant to establish prognosis and treatment and for research purposes.

An unusual case of endomyocardial fibrosis is reported complicating an idiopathic hypereosinophilic syndrome. Persisting hypereosinophilia, degranulated eosinophils in the blood, and myocardial activity have been found accompanying the fibrotic phase of endomyocardial disease. This occurrence supports the unitarian theory on tropical and temperate endomyocardial disease and suggests in such a condition the use of steroids or cytotoxic drugs in addition to surgery.

Background— Fabry cardiomyopathy is diagnosed by detection of left ventricular hypertrophy (LVH) in patients with α-Galactosidase A deficiency. Conventional noninvasive tools are unable to provide a preclinical diagnosis allowing prompt institution of enzymatic therapy. Methods and Results— We studied three groups of patients: 10 patients with causal mutations for Fabry disease and LVH, 10 mutation-positive patients without LV, and 10 healthy relatives without causal mutations and no LVH. All patients with LVH and 6 patients with Fabry disease without LVH with complex repetitive ventricular arrhythmias underwent biventricular endomyocardial biopsy to assess cardiac involvement. In all patients 2-dimensional echocardiography with tissue Doppler analysis in the pulsed Doppler mode was performed: systolic (Sa), early diastolic (Ea), and late diastolic (Aa) velocities were measured, and the Ea/Aa ratio and the dimensionless parameter E/Ea were computed at both corners of the mitral annulus. Histology and electron microscopy studies showed glycosphingolipid deposits in all cases. All mutation-positive patients had significant reduction of Sa, Ea, and Aa velocities at both corners of the mitral annulus compared with normal control subjects. Ea/Aa ratio was significantly lower and E/Ea ratio significantly higher in mutation-positive patients than in control subjects. Patients with LVH showed significantly lower contraction and relaxation tissue Doppler velocities, lower Ea/Aa ratio, and higher E/Ea ratio in comparison with mutation-positive patients with no LVH. Conclusions— Fabry cardiomyopathy is characterized by reduced myocardial contraction and relaxation tissue Doppler velocities, detectable even before development of LVH. Tissue Doppler imaging can provide a preclinical diagnosis of Fabry cardiomyopathy, allowing early institution of enzyme replacement therapy.