Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Relative Cross-sectional area Differences" (RCD) and "Relative Velocities of Contraction" (RVC) permit a differentiation between normal subjects and patients with different degrees of myocardial failure, as previously described. Important determinants of the parameters RCD and RVC are changed, if ventricular volume and stroke volume increase and heart rate decreases, as is commonly observed in athletes. Examinations were performed at rest and after exercise on 31 athletes and 33 untrained normal subjects. Ventricular volumes were clearly increased in athletes. RCD, however, which is an equivalent to the ejection fraction, showed only slight alterations with physical training. RVC was obviously not changed by athletic training. After exercise athletes showed a significant increase in RCD. In untrained subjects only small changes in RCD were observed. In conclusion, the results show that RCD and RVC can quantitatively assess the degree of myocardial failure in cases of left ventricular dilatation without having to take into account the patients' degree of physical training.
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PMID:[Heart diagnosis using M-mode-echocardiography. Continuous registration of the left ventricular transversal internal diameter. III. Measurements on highly trained athletes (author's transl)]. 14 May 48

Diastolic wall stress and compliance were determined in 74 patients with essential hypertension during diagnostic cardiac catheterization. Ventricular compliance was normal in compensated essential hypertension without coronary artery disease even at severe left ventricular hypertrophy. In contrast, additional coronary stenosis and ventricular dilatation due to cardiac decompensation was asscociated with considerable decrease in ventricular compliance. Thus, left ventricular hypertrophy in essential hypertension does not imply per se a change in ventricular compliance. A decrease in ventricular compliance was followed by a decrease of forward pump function of the left ventricle. whereas ventricular work index (as estimated as the product out of systolic wall stress and the stroke volume) increased. This disproportion between external and internal ventricular work increased with increasing ventricular dilatation and was greatest in decompensated essential hypertension. Accordingly, decompensated essential hypertension had largest ventricular work load and lowest forward pump function in comparison to all other patient groups with essential hypertension. The mass to volume ratio may be considered an important determinant of the degree of left ventricular hypertrophy in essential hypertension. The relationship between the mass to volume ratio and the systolic wall stress may provide a diagnostic and prognostic evaluation of the left ventricle in essential hypertension on the basis of dynamic ventricular geometry.
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PMID:[The heart in hypertension. III. Determinants of left ventricular hypertrophy and diastolic left ventricular compliance (author's transl)]. 15 7

The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.
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PMID:Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area. 44 20

Maximal changes in haemodynamics and segmental wall motion were seen 2 min after coronary occlusion and were examined in relation to the loading conditions of the left ventricle before occlusion in 20 open chest dogs. There was a significant inverse relationship between the preligation mean aortic pressure and the percentage decrease in stroke volume following ligation. This relationship was observed whether afterload was distributed randomly (mean aortic pressure ranging from 9.7 to 17.6 kPa [73 to 132 mmHg]) between all dogs (r = 0.65; P less than 0.001) or altered by methoxamine (+4 kPa [+30 mmHg]) and nitroprusside (-3.2 kPa [-24 mmHg]) within the same dog (r = 0.82; P less than 0.001; n = 8). Although occlusion of the anterior descending artery caused a small (+5.5%) but significant increase in end-diastolic length of the non-ischaemic epicardial segment, the capacity for compensatory ventricular dilatation was not dependent on preligation afterload. However, the capacity of the ischaemic segment to undergo systolic expansion was significantly greater (+30.2% of end-systolic segment length) in those dogs with the lowest preligation MAP (8 to 12 kPa [60 to 90 mmHg]) compared with systolic lengthening of only 15.8% in the high afterload group (15 to 18 kPa [112 to 135 mmHg]). These data indicate that the loading conditions of the left ventricle predetermine the extent of global and segmental left ventricular dysfunction during the early phase of acute ischaemic injury.
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PMID:Afterload as a predeterminant of haemodynamics and segmental wall motion following coronary artery occlusion. 47 39

Echocardiography was used to examine the extent and significance of impairment in left ventricular function in 20 patients with rheumatic mitral stenosis. Indices of left ventricular performance--normalised mean rate of circumferential fibre shortening (Vcf), ejection fraction, normalised posterior wall velocity, and stroke volume were reduced. The impairment in left ventricular function was related to the degree of functional disability (NYHA), right ventricular dilatation, and left atrial enlargement. Vcf was inversely related to both the internal right ventricular diameter (r=-0.767, P less than 0.001) and the degree of left atrial enlargement (r=-0.554; P less than 0.05). The normalised velocity of the interventricular septum and the maximum systolic and diastolic endocardial velocities were also reduced. These results suggest that abnormalities in contractility of left ventricular myocardium are responsible for the impaired myocardial function in patients with mitral stenosis and that such impairment is clinically significant.
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PMID:Left ventricular function in rheumatic mitral stenosis. Clinical echocardiographic study. 51 75

Twenty-four patients with aortic valve disease were studied before and 19+/-12 months following valve replacement with a well functioning prosthesis. Biplane left ventricular angiography and pressures were utilized to determine end-diastolic volume/m2 (EDV), end-systolic volume/m2 (ESV), ejection fraction (EF), left ventricular mass/m2 (LVM) and stroke work (SW). There were nine patients with aortic stenosis (AS), ten patients with combined stenosis and regurgitation (AS-AR), and five patients with aortic regurgitation (AR). Following surgery, patients with regurgitation preoperatively showed marked regression in EDV and ESV. All groups demonstrated regression in LVM. Fifteen patients with a normal EF preoperatively (65+/-11%) had no change after surgery; the nine patients with a low EF before surgery (38+/-8%) had a normal EF after surgery (60+/-16%). We conclude that left ventricular dilatation, hypertrophy, and reduced left ventricular pump function are largely reversible after successful aortic valve replacement.
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PMID:Left ventricular function before and following aortic valve replacement. 92 63

Deletions and point mutations of mitochondrial DNA (mtDNA) of patients with dilated or hypertrophic cardiomyopathy were analyzed using the polymerase chain reaction and fluorescence-based direct sequencing. The patients included are with hypertrophic cardiomyopathy associated with left ventricular dilatation, a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and a patient with fatal infantile cardiomyopathy. Deletions were frequently seen in mtDNA in patients with dilated cardiomyopathy. The mtDNA was sequenced and the direct repeat at each edge of deletion was identified as (5'-CATCAACAACCG-3') which was located in the ATPase6 gene and in the D-loop region. In a patient with hypertrophic cardiomyopathy associated with left ventricular dilatation, another mutant mtDNA was found not to have directly repeated sequence, and was revealed to jump from nucleotide position 8,992 to position 16,072 of mtDNA resulting in a 7,079 bp deletion. This patient had unique point mutation in the tRNA genes. A G-to-A transition in the tRNA(Cys) gene (nucleotide position 5,821) at the aminoacyl acceptor stem and an A-to-G transition in the tRNA(Thr) gene (nucleotide position 15,951) were identified. In a patient with MELAS, an A-to-G transition in the tRNA(Leu)(UUR) gene (nucleotide position 3,243) was observed. This mutation was located at the 5' end of the dihydrouridine loop of this tRNA molecule, and would disturb its function. In a patient with hypertrophic cardiomyopathy associated with lactic acidosis, mutations of mtDNA should be suspected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial DNA mutations in cardiomyopathy. 143 21

Serial electrocardiograms as well as echocardiographic studies of 51 pilgrims suffering from acute heat stroke (mean rectal temperature 41.6 degrees C) were performed. All patients were examined immediately after cooling and 24 h later whenever possible. Regional wall motion abnormalities were detected in 9 cases (17.6%) while pericardial effusion was observed in 13 cases (25%) and asymmetrical septal hypertrophy was detected in 8 cases (15.6%). Other cardiac abnormalities included right ventricular dilatation and increased in left ventricular internal dimensions in 4 cases (7.8%), respectively. Thirteen cases (25.5%) had normal echocardiographic findings. Forty (78%) patients had sinus tachycardia while 8 cases (15.7%) showed atrial fibrillation with uncontrolled ventricular rate, and 3 (5.8%) had sinus bradycardia. Heat stroke electrocardiograms showed tracings demonstrating ST segment depression, compatible with ischaemia in 9 cases, while in 6 cases there were nonspecific T wave changes, whereas in another 4 cases the tracings demonstrated different conduction abnormalities. The collected data were analysed and compared to those of 43 control patients. The adverse effects of heat stroke on the heart are multifactorial requiring the utmost attention and understanding, as they reflect the patient's cardiovascular status.
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PMID:Non-invasive evaluation of cardiac abnormalities in heat stroke pilgrims. 145 70

Survival after myocardial infarction decreases with left ventricular dilatation, although dilatation at 4 weeks was found to be compensatory. To study this apparent discrepancy, prospective simultaneous volume and hemodynamic measurements at rest were extended in 39 patients with small and 37 with large myocardial infarctions from 4 (range 2 to 6) days and 4 (range 3 to 5) weeks to 6 (range 5 to 8) months after myocardial infarction and were repeated during exercise. In small myocardial infarctions, end-diastolic volume index (EDVI) decreased from 4 days to 6 months; ejection fraction, stroke volume index (SVI), and end-systolic volume index (ESVI) remained unchanged. SVI increased during exercise at 4 weeks and at 6 months. In large myocardial infarctions (n = 37) ESVI (4 days = 38 +/- 3, 4 weeks = 47 +/- 3,* 6 months = 52 +/- 3*; *p less than 0.05 versus 4 days) and EDVI (4 days = 72 +/- 3, 4 weeks = 86 +/- 5,* 6 months = 92 +/- 5* ; *p less than 0.05 versus 4 days and p less than 0.05 versus 4 weeks) increased at constant wedge pressure. SVI remained unchanged beyond 4 weeks (4 days = 35 +/- 2, 4 weeks = 42 +/- 2*, 6 months = 42 +/- 2*; *p less than 0.05 versus 4 days) and increased during exercise at 4 weeks (rest = 45 +/- 2, exercise = 55 +/- 3; p less than 0.05) but not at 6 months (rest = 42 +/- 3, exercise = 45 +/- 3; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Compensatory and noncompensatory left ventricular dilatation after myocardial infarction: time course and hemodynamic consequences at rest and during exercise. 173 73

Based on animal experiments in rats (spontaneous and renal hypertension, experimental aortic stenosis, thyroxine and training-induced hypertrophy, and aorto-caval fistula with and without additional unilateral renal artery coarctation) as well as clinical data and literature, the functional consequences of cardiac hypertrophy and structural ventricular dilatation are analyzed and discussed. A methodological approach, developed on the basis of Frank's diagram and model calculations, permits quantitatively estimating the significance of ventricular geometry (wall thickness and inner dimensions) compared to myocardial alterations (decrease in contractility and distensibility) and hemodynamic load (preload and systolic pressure). As a rule, hypertrophy causes an increase in ventricular working capacity, which allows the heart to cope with an increased hemodynamic load without a decrease in stroke volume and without enhanced systolic stress requirement. Adverse consequences mainly concern ventricular compliance, cardiac energetics, and electrophysiological parameters. Particularly from the example of the aorto-caval fistula, it can be seen that enhanced systolic wall stress does not necessarily lead to heart failure within a few months. However, the length of time for which the additional wall stress, with correspondingly increased energy demand, can be tolerated remains to be determined. In later stages, a multitude of alterations on the cellular, tissue, and organ level occurs, affecting myocardial and ventricular mechanics and energetics, depending on the type, velocity of development, and duration of overload. A distinction should be made between the adverse alterations, which can be related to myocardial growth, and those that are not necessarily related to a certain cell size (receptors, transformation of the contractile proteins) as well as those changes that do not primarily influence the myocardial cell (arteriosclerosis, microangiopathy). Structural dilatation alone could lead to insufficiency only in the case of substantial increase in inner ventricular radius. Reduced contractility, myocardial distensibility, and increased pressure load aggravate the negative effects of dilatation in a predictable manner, as demonstrated on the basis of a representative case of dilative cardiomyopathy. Using the example of spontaneously hypertensive rats, it is shown that ventricular mass and shape are differently influenced by various blood-pressure lowering agents, e.g., atenolol, nifedipine, and dietary interventions. It is concluded from the analysis of chronic cardiac reactions that adaptive processes are, in principle, ambiguous in character, revealing negative components even in the case of regular adaptation. However, it seems unjustified to aim at a regression of hypertrophy without reducing the underlying hemodynamic overload.
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PMID:Functional consequences of cardiac hypertrophy and dilatation. 182 78


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