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Experimental cardiomyopathy in terms of heart hypertrophy and noninflammatory myocardial lesions was induced in rabbit by i.v. administration of anthracycline antibiotic daunorubicin during 2 to 12 weeks. The animals showed a high rate of unexpected mortality in comparison with controls. This mortality was evaluated from the point of view of the unexpected death as a forensic pathologic term.

The hydroxyproline concentration, representing collagen content, has been investigated in normal and hypertrophied rat hearts. Enlargement of the heart was produced by four methods: In spontaneously hypertensive rats the free wall of the right and left ventricles and the septum were analyzed separately. Furthermore, the left ventricular free wall was divided into endomyocardial and epimyocardial slices to permit separate investigation. Otherwise, the hydroxyproline concentration was always analyzed in left ventricular tissue. In swimming rats the absolute heart enlargement was very slight (15%), whereas the hydroxyproline concentration remained unchanged. The degree of hypertrophy was greater in all other experimental animals and was associated with an increase in hydroxyproline concentration in hypertrophied tissue. There was a positive correlation between the rate of hydroxyproline concentration increase and the degree of hypertrophy. The findings only vary in different experimental groups of Goldblatt rats at an early stage. Four weeks after surgery we found a left ventricular hypertrophy of 34%, whereas hydroxyproline concentration in left ventricular tissue was unchanged in comparison to control values. In spontaneously hypertensive rats the increase in hydroxyproline concentration in endomyocardial areas was considerably greater than in epimyocardial areas. Significant differences in water retention and nitrogen content (µg/mg dry tissue) of hypertrophied and normal ventricular tissue were not found.

1. The effects of chronic dietary salt-loading and nifedipine therapy on hypertension-prone (SBH), -resistant (SBN) and parental (SB) Sabra rats were investigated. Salt diet for 12 weeks resulted in a sustained hypertension and heart hypertrophy only in SBH. 2. Nifedipine therapy (300 p.p.m. = 300 mg/kg of food) introduced after week 7 on a salt diet, achieved small changes in salt-loaded SBN and SB rats, but resulted in a marked decrease in blood pressure in SBH rats within 1 week and in a regression of cardiac hypertrophy. 3. Plasma renin activity rose slightly in nifedipine treated SB and SBN rats, but decreased significantly in treated SBH rats. 4. Histopathological investigations revealed hypertensive vasculopathy in three out of nine untreated SBH rats, whereas there were no morphological changes in the treated rats.

Abdominal aorto-caval fistula was experimentally induced in rats, and animals were sacrificed 5 days, 1 month, and 6 months later. Cardiac weight almost doubled the normal weight during the first month. Cell length increased to the same extent as the cell width, indicating harmonious growth. Increase in cell volume, as well as the amount of degenerative changes, were more pronounced in subendocardium than in midwall and subepicardium. Cytological features of active cellular growth was found not only in the early stages (5 days and 1 month) but also 6 months after the operation. This finding is consonant with proteosynthesis stimulation not only in the early period of constitution of hypertrophy but also in the later stages.

A NaCl load in chronically hypoxic rats abolished the increase in plasma renin activity occurring in rats exposed to hypoxia of the same degree and duration but with normal NaCl intake. The parallel reduction in hypoxic hypertrophy of the right ventricle in NaCl-loaded rats could be considered as indirect evidence supporting the view that renin may be involved in the development of heart hypertrophy.

Vergleichende histologische Messungen uber die Herzmuskelfasergrose der rechten und linken Kammer an totenstarren und chloroformstarren Katzenherzen zeigen, das die Totenstarre auf beide Ventrikel gleich einwirkt. An 60 Menschenherzen wurde die mittlere Faserbreite an der Basis der rechten und linken Kammer ermittelt, errechnet aus 70 000 mikroskopischen Einzelmessungen. Es ergibt sich, das die Muskelfasern der linken Kammer durchschnittlich um 25% breiter sind als die der rechten. Bei der Hypertrophie einer Kammer nimmt entsprechend dem Grad der Hypertrophie die Muskelfaserbreite zu. Dies gilt fur die Hypertrophie der linken wie der rechten Kammer. An 20 Menschenherzen wurde einerseits am rechten, andererseits am linken Ventrikel die Faserbreite an der Herzspitze und Herzbasis der gleichen Kammer verglichen. Auf Grund der angestellten histologischen Messungen fanden sich gleiche Faserbreiten an Basis und Spitze der Kammern nichthypertrophischer Herzen, grosere Muskelfasern an der Spitze der jeweils hypertrophischen Kammer.

1. 1. Four fatal cases of unexplained hypertrophy and dilatation of the heart during the third decade of life are presented. None of the usual causes of hypertrophy were present. 2. 2. The onset of illness differed in individual cases and was not at first recognized as heart disease. 3. 3. Electrocardiograms at first were normal. When changes occurred, the abnormalities suggested only nonspecific myocardial damage. 4. 4. The possible etiologic factors are discussed, but it is not concluded which, if any, were responsible for the cardiac hypertrophy. 5. 5. There is no certainty that the causes of heart disease in the four cases were related.

This case is reported for the following reasons: 1. The aneurysm is an unusually large one. 2. An opportunity is given to observe the progressive increase in size which an aneurysm may undergo in one year. 3. The destructive force of a pulsating, blood-filled aneurysmal sac is well illustrated. Case No. 23,545, Emory University Division, Grady Hospital, Atlanta, Georgia. H. T., colored laborer; age 37; chief complaint, “knot in left side; pain through the heart.” Admitted February 14, 1927. Family history, negative, Marital history, married twice. (First wife died with miscarriage; no children by second wife.) Past history, negative. Present illness: Onset in January, 1926, with dyspnea, and pain in left chest and back. Most severe over precardium and in left axilla. Admitted to Medical Clinic, Out-patient Department, on February 23, 1926, complaining of pain in left side, over lower sternum and axilla. Physical examination showed a heart hypertrophy to the left and downward. On February 26, 1926, fluoros...

Bei einem 5jahrigen Madchen wird eine wahre, besonders linksseitige Herzhypertrophie mit Verdoppelung des Herzgewichtes bei schleichender Myokarditis mikrometrisch festgestellt. Zur Frage der sog. idiopathischen Herzhypertrophie wird Stellung genommen und diese Herzhypertrophieformen werden als myokarditische Hypertrophien gedeutet. Als Ursache der Hypertrophie wird eine vermehrte Faserspannung infolge myogener Dilatation angenommen. Die Annahme vonMoritz, wonach auch eine myogene Dilatation, vorausgesetzt, das sie lange genug besteht, zum Ausgangspunkt einer Hypertrophie werden kann, wird durch unseren Fall erstmalig bestatigt.

Myocyte enhancer factor (MEF2) are MADS box transcription factors that play important roles in the regulation of myogenesis and morphogenesis of muscle cells. MEF2 proteins are activated by mechanical overload in the heart. In this study, we found the interaction of MEF2C with the regulatory protein Ki-1/57 using yeast two-hybrid system. This interaction was confirmed by GST-pull down assay in vitro and by co-immunoprecipitation in vivo. This interaction is also dependent on pressure overload in the heart. Co-imunoprecipitation assay with anti-MEF2 and anti-Ki-1/57 antibodies demonstrated a basal association between these proteins in the left ventricles of control rats. Pressure overload caused a reduction in this association. Ki-1/57 co-localizes with MEF2 in the nucleus of myocytes of control rats. However, after submitting the animals to pressure overload Ki-1/57 leaves the nucleus thereby decreasing this co-localization. Ki-1/57 also exerts an inhibitory effect upon MEF2C DNA binding activity. These results suggest that Ki-1/57 is a new interacting partner of MEF2 protein and may be involved in the regulation of MEF2 at the onset of hypertrophy.

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:28:22Z No. of bitstreams: 0 Made available in DSpace on 2014-05-27T11:28:22Z (GMT). No. of bitstreams: 0 Previous issue date: 2013-02-10 Background: Currently, 13-cis-retinoic acid (13-cis-RA) is the most effective therapy for acne. Isotretinoin, a first-generation synthetic 13-cis-RA compound, is associated with numerous adverse effects. To investigate the cardiac effects of 13-cis-RA, acne patients receiving 13-cis-RA were studied. Methods: Twenty male patients with acne were enrolled in the study. Patients were treated with a dose of 0.5 mg/kg/d of isotretinoin. All participants were assessed prior to treatment and after 10 weeks of therapy with Doppler-echocardiogram. Results: Patients showed reductions in right atrium vertical diameter, left atrium longitudinal diameter, left atrium volume and left ventricular diastolic diameter over the course of treatment. Significant increases in interventricular septum diastolic thickness, posterior wall diastolic thickness, relative wall relative thickness and left ventricle (LV) mass were observed. The LV mass index showed an increase in ventricular mass and a decrease in the cavity size. Examining LV systolic function, a decrease was observed for the cardiac index. Conclusion: In this study, 10 weeks of 13-cis-RA therapy at a dose of 0.5 mg/kg/d was found to promote concentric-type heart remodeling due to the occurrence of two associated events: heart hypertrophy and hypovolemia. © 2011 Elsevier B.V. All rights reserved. Department of Internal Medicine Botucatu Medical School UNESP, Sao Paulo Department of Dermatology Botucatu Medical School UNESP, Sao Paulo Department of Internal Medicine Botucatu Medical School UNESP, Sao Paulo Department of Dermatology Botucatu Medical School UNESP, Sao Paulo

In the natural history of the development of hypertension rats have problems with the elimination of sodium, in the initial phase. We speculated that this is probably due to increased renovascular resistance in the early stage, so that the rats probably need an increase in perfusion pressure to overcome this. They need to switch on the so-called pressure natriuresis. However, the increase in perfusion pressure is not without consequences. The blood pressure increase produces an autoregulatory vasoconstriction in the kidney, so that the renovascular resistance increases again (Fig. 1).

Myocardial contractile function was assessed in a chronic, slowly developing hypertrophy in pigs in order to approximate more closely the situation seen in patients with heart hypertrophy due to pressure overload. Presence of heart hypertrophy was confirmed 4 and 8 weeks after the surgery by increased wall thickness and intercapillary distances. Peak developed force at different resting loads as well as +dp/dt and −dP/dt of the trabecular muscle strips did not change at 4 weeks, but these parameters were significantly depressed in the 8-week hypertrophied heart. Positive force-frequency relationship was significantly improved in the 4-week group and depressed or even negative at 8 weeks. It is suggested that a reduction in the contractile performance of the hypertrophied hearts at late stages may be due to combination of factors such as reduced fibre shortening because of increased wall stress and an intrinsic depression of the inotropic state subsequent to changes in subcellular-control mechanisms.

Experiments were conducted in copper deficient male and female rats fed diets containing fructose or starch in order to determine whether the same type of interaction between copper status and dietary carbohydrate found in male rats also occurs in the female rat. Mortality occurred only in the male rats fed the fructose diet deficient in copper with 40% of the animals dying during the 8 week study. Only anemia, hypercholesterolemia, increased BUN, heart hypertrophy and reduced body weight were observed in these animals which could be related to their mortality. Despite the increased mortality, plasma ceruloplasmin, erythrocyte SOD and hepatic copper concentrations were reduced to a similar extent in all rats regardless of the sex of the animals or of the type of dietary carbohydrate fed. The results of the present study indicate that although direct measurements of copper status of female rats fed fructose diet deficient in copper are similar to their male counterpart, they are apparently protected from the lethal consequences of the deficiency.

The chronical exposure of young rats to a simulated altitude of 3500 m results in number of functional adaptations (Grandtner et al., 1974; Turek et al., 1972a). As concerns the heart, a multiplication of capillaries have been noted under chronical hypoxia (Turek, 1972b); Friedman et al., 1973). The stay in the hypoxic chamber leads also to an increase of the heart weight (heart hypertrophy). However, the extent of the latter can vary considerably: in rats born and rised in the hypoxic conditions (“natives”) a bilateral cardiac hypertrophy regularly occurs (Turek et al., 1972b). In those born at sea level and exposed to the same hypoxia fran their youth only (“newcaners”), the increase of the heart weight is restricted exclusively to the right ventricle (Grandtner et al., 1974). In addition, the hearts of the above two groups differ from functional point of view. While in the “natives” the cardiac output is 50 per cent depressed, it is elevated in the “newcaners” (Turek et al., 1972a). The amount of kinetic work supplied by 1 g of the left ventricular myocardium is therefore significantly higher in hearts of the latter animals. This elevated work output of the heart is apparently enabled by higher rates of the oxidative energy production. An increase in the glycolytic fluxes (Hochachka et al., 1977) as well as the accumulation of respiratory enzymes in heart homogenate (Shertzer et al., 1972; Tappan et al., 1957) may underlie such an adaptation to chronical hypoxia. In this work we tried to assess the kinetic aspects of mitochondrial function using the optical methods developed by Chance (Chance, 1976; Sugano et al., 1974). The hearts from rats exposed to the early (“natives”) and to the late (“newcomers”) hypoxia were compared. The left ventricular vascularization was also studied in these two groups by a new morphanetric approach (Rakusan et al., 1980) derived from the work of Loats et co-workers (Coats et al., 1978).

The purpose of the study was to investigate the possibilities of flow cytometry (FCM) for the analysis of DNA polyploidy in human heart tissue. Suspensions of single nuclei were prepared with the detergenttrypsin procedure and stained with propidium iodide. A mathematical correction procedure was developed to correct for background and clumping. For diploid model populations of chicken and trout red blood cells this correction reduced artifactual fractions in the FCM DNA profile to less than 0.5%, indicating that interference by background and clumping was almost completely overcome by this correction procedure. FCM DNA profiles were obtained from 12 hypertrophic and 7 normal human adult hearts. Clear differences were found between the DNA profiles from the normal and the hypertrophic hearts, the latter showing a higher degree of polyploidization. From the corrected DNA profiles, six different polyploidization parameters were computed, all of which showed a significant correlation with at least three out of four different parameters for heart hypertrophy. FCM appears to be a reliable method for the measurement of polyploidization in heart tissue, provided background and clumping are corrected for.

There is perhaps no problem in medicine of greater interest to clinician and pathologist alike than that of the relation which some of the more important manifestations of chronic nephritis, as vascular hypertension, heart hypertrophy, uremia and edema, bear to the renal lesion itself. During the past summer, having in view an experimental study of some phases of vascular hypertension, I undertook a critical review of the general literature of renal physiology and pathology, and was amazed, not only at the multiplicity of theories concerning the relation of the kidney to heart hypertrophy and hypertension, but also at the importance attached by many writers to the part played by the hypothetical internal secretion of the kidney. I use the term "hypothetical" advisedly, for, although certain clinical observations are very suggestive, the experimental basis on which the theory rests appeared to me to be most unstable. Further study of

WHEN medical terminology was less precise the expression "strained heart" was employed at times to describe obscurely but ominously diseased hearts. This diagnosis is no longer made, but currently ...

This study evaluates the effect of propranolol 10 to 20 mg per os, on so-called nonspecific S-T segment and T-wave changes in patients suspected of having coronary insufficiency. One hundred forty three subjects were tested. Of these, 41 patients with definite heart disease (31 coronary patients and ten with left heart hypertrophy and strain) served as a control. One hundred two patients with nonspecific S-T-T changes to be evaluated were divided into two subgroups according to their clinical history: 53 of these patients had no clinical history of heart disease and had precordial pain clinically not suggestive of coronary insufficiency; 49 patients, in whom, on clinical grounds, the diagnosis of coronary insufficiency remained doubtful and angina pectoris could not be definitely excluded. No patients in the control group reverted to normal ECG patterns after propanolol. In most subjects in whom, on clinical grounds, angina pectoris could be excluded, the ECG pattern reverted to normal. In the doubtful cases, both clinically and electrocardiographically, a good separation of coronary from noncoronary could be established. The mode of action and the rationale of this test, as well as its clinical significance, are discussed.

Introduction: Biallelic truncating variants in ALPK3 have recently been described to cause pediatric cardiomyopathy (CMP). Functional studies have found disorganized intercalated discs and sarcomeres and calcium mishandling in both patients and mutant stemcellderived cardiomyocytes. Objectives: To delineate the clinical and genetic spectrum of ALPK3related disease and study genotypephenotype correlations. Methods: We collected clinical and genetic data on ALPK3related CMP patients, and performed ALPK3 staining in heart and skeletal muscle of 3 individuals carrying biallelic truncating variants. Results: We report biallelic ALPK3 mutations for a total of 18 patients: 9 previously reported cases and 9 novel patients from 6 families. Nine patients had biallelic truncating variants, 7 had a truncating and a missense variant, and 1 had a homozygous missense variant in ALPK3. Nine of 16 liveborn patients showed (biventricular) DCM during neonatal life that transitioned to predominantly HCM with surveillance. Several patients showed extracardiac features, including short stature (8/13), contractures (6/15), severe scoliosis (5/12), cleft palate (CP) or velopharyngeal insufficiency (5/15), and dysmorphic (Noonanlike) facies (8/14). Biopsy of 4 patients showed focal cardiomyocyte hypertrophy, subendocardial fibroelastosis

s. Internal illnesses. Heart in chronic respiratory diseases according to prof. Lurdwig'y Braun'y (Die arztliche Praxis, No. 2-1930) undergoes secondary changes in the following sequence: right ventricular hypertrophy, its dilation, right atrial hypertrophy, its dilation, and finally, or at the same time, left heart hypertrophy with its subsequent dilation.

The Republic of Colombia, located at the northwestern corner of South America, is a tropical country. For this reason there are no seasonal changes in the whole of its territory, as there are in the Temperate Zone. The temperature is uniform all through the year in all the cities, but it varies in accordance with the altitude above sea level at which they are located. It is therefore erron eous to believe, as some residents of the Temperate Zone do, that every tropical city enjoys a hot climate. This is true only of those that are located at sea level. As the altitude increases the temperature drops, and it is for this reason that the city of Bogota, the capital of Colombia, built on a plateau at 8,016 feet (2,440 meters) above sea level, has a normal temperature of 14.55 C. (58 F.); that is to say, a relatively cold