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PubMed2002

[Importance of tumor necrosis factor-alpha in the pathogenesis of heart failure].

Clinical and experimental evidence demonstrating the effects of tumor necrosis factor-alpha (TNF-alpha) in patients with heart failure continues to accumulate. It is well established that high concentrations of TNF-alpha appear in the circulation of patients with heart failure and that these levels have a directly proportional correlation with the patient's functional class. TNF-alpha levels also show a linear relation with prognosis. These circulating levels are responsible for the decreased expression of myocardial TNF-alpha receptors observed in heart failure. As a result of extrapolation of findings from experimental animals, we assume that TNF-alpha is deleterious to myocardial function in humans because it induces a negative inotropic state in patients who have not undergone heart transplant. Supporting this assumption is the fact that the resolution or improvement of pressure overload (obstructive hypertrophic myocardiopathy, by ethanol ablation) and volume overload (terminal dilated myocardiopathy, by ventricular assistance) states is accompanied by a decrease in myocardial TNF-alpha expression. The use of specific antagonists of circulating TNF-alpha in patients with symptomatic heart failure has been demonstrated to be safe and possibly effective. At present, multicenter studies are under way to assess the efficacy of this antagonism in a larger number of patients. If the results of these studies are favorable, we will have new therapeutic elements for managing patients with advanced hear failure. The transplanted heart behaves differently from the native heart. From the early stages of HTx, myocardial TNF-alpha expression is greatly increased (much more than in patients with heart failure) and not associated with contractile dysfunction, in contrast with what occurs in the native heart. However, we know that the transplanted heart soon develops ventricular hypertrophy, fibrosis, diastolic dysfunction, and late graft failure, even in the presence of normal epicardial coronary arteries. Clinical evidence suggests that TNF-alpha may be involved in these processes.

Heart Failure↗
PubMedDate not supplied

[The plasma level of an inactive moiety of B-type natriuretic peptide precursor as a predictor of cardiac function during operations under extracorporeal circulation].

Ventricular cardiomyocytes secrete brain natriuretuc peptide (BNP) and an inactive moiety of its precursor (nt-proBNP). It is recommended the blood level of the latter should be monitored to ascertain the severity of myocardial lesion. This investigation was undertaken to study the diagnostic and prognostic value of a substantial increase in blood nt-proBNP levels (600 pg/ml or more) in patients operated on under extracorporeal circulation. Thirty-eight patients operated on for coronary heart disease were examined. Before surgery, the plasma concentration of nt-proBNP had been determined by electrochemiluminescence (Elescys, Roche). According to plasma nt-proBNP levels, the patients were divided into 2 groups: 1) 24 patients with nt-proBNP levels of less than 600 pg/ml; 2) 14 patients with its levels of 600 pg/ml or more. Group 1 patients showed signs of diastolic dysfunction of the right ventricle: the lower ratio of its early to atrial filling linear velocity integrals and the increased end-diastolic volume index. In the postperfusion period, nt-proBNP is a significant independent predictor of left ventricular function. The patients with the baseline nt-proBNP levels of above 600 pg/ml were found to have decreases in ejection fraction of the left ventricle and in its pump ratio along with elevated pulmonary wedge pressure.

Adult↗
PubMed2004

[Evaluation of diastolic function by transmitral color M-mode flow propagation velocity in hypertensive patients].

OBJECTIVE: Diastolic dysfunction is considered as the most important cause of heart failure and morbidity in hypertensives. This study was designed to evaluate the relationship between the transmitral diastolic color M-mode flow propagation velocity (FPV) and left ventricular relaxation by using Doppler echocardiography. METHODS: In the present study, thirty-nine patients (21 male, 58.3%, age mean 52.7+/-5.9 years) with hypertension stage-I and over, were included. Transmitral diastolic E and A velocities, E-deceleration time (DT) and isovolumic relaxation time (IVRT) were measured by pulse Doppler method. We performed color M-mode technique for measurement of FPV of transmitral diastolic flow in the apical four-chamber view. We measured slope of aliasing velocity (blue aliasing) determined by color M-mode images. RESULTS: Flow propagation velocity values were not statistically related with age and gender, whereas differentiation of age groups were estimated as poor parabolic relationship, specially in patients over fifty years, FPV is estimated to be decreasing. Color M-mode FPV is correlated with DT, (r=-0.715, p<0.01), IVRT (r=-0.736, p<0.01) and interventricular septum thickness (r=-0.498, p<0.01), but not correlated with E/A ratio. CONCLUSION: Color M-mode FPV is correlated with DT and IVRT, which are important parameters for evaluation of diastolic function in hypertensive patients. This parameter is related with left ventricular relaxation and should be considered as a routine echocardiographic evaluation, because it is not affected by minimal changes in left ventricular filling pressure.

Adult↗
PubMed2004

Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis.

BACKGROUND: It is not known whether multivessel coronary spasm occurs spontaneously in patients who have variant angina (VA) with demonstrated multivessel spasm induced by intracoronary injection of acetylcholine (ACh). Regional left ventricular (LV) diastolic dysfunction or wall motion abnormality may persist after an episode of coronary vasospasm. Color kinesis (CK) is a recent development that facilitates the echocardiographic evaluation of regional diastolic wall motion. METHODS AND RESULTS: Regional diastolic wall motion was evaluated using CK in 26 patients with VA within 1 week of the last episode of angina. The LV segmental filling fraction in the short-axis view during the first 30% of the diastolic filling time, expressed as a percentage, was used to objectively identify postischemic diastolic endocardial motion asynchrony. Diastolic asynchrony or regional LV delayed relaxation was noted in all 26 (100%) patients and in 14 (54%) it was detected in multiple vascular territories, suggesting multivessel spasm. Multivessel spasm was induced by ACh in 11 (79%) of the patients with suspected multivessel spasm by CK. In 11 (92%) of the 12 patients with multivessel spasm induced by ACh multiple regions of delayed relaxation had been noted by CK. The regions of delayed relaxation were largely consistent with the territories perfused by the arteries reacting to ACh (sensitivity: 96%, specificity: 91%). CONCLUSION: ACh induced spasm in the same coronary arteries as those perfusing the regions with delayed diastolic wall motion detected by CK in most of the patients with VA, suggesting that multivessel spasm does occur spontaneously in patients with susceptible arteries.

Acetylcholine↗
PubMed1998

[Evolution of the filling pattern of the left ventricle during the first year after an acute myocardial infarct. The influence of the infarct size].

OBJECTIVES: Acute myocardial infarction induces diastolic dysfunction as a result of the alteration of left ventricular relaxation and stiffness caused by ischemia and fibrosis. This study analyzes the association of infarct size with the diastolic filling pattern and the evolution of the latter during the first postinfarction year. PATIENTS AND METHODS: The study group consisted of 68 patients with a first acute myocardial infarction treated with thrombolytic agents. A Doppler echocardiography was performed at 8 +/- 2, 32 +/- 7 and 370 +/- 23 days after infarction. Five measurements of the ratio between E and A waves peak velocities (E/A ratio) and of the E deceleration time (EDT, ms) were averaged in each echocardiographic study. The patients were divided according to infarct size into a large infarct group (creatine kinase > 1,000 U/ml; 1,913 +/- 883; n = 26) and a small infarct group (creatine kinase < 1,000 U/ml; 556 +/- 227; n = 42). RESULTS: The large infarct group exhibited a greater E/A ratio and shorter EDT than the small infarct group in the first week (E/A ratio: 1.4 +/- 0.7 vs 0.8 +/- 0.3; p = 0.0001; EDT: 159 +/- 49 vs 192 +/- 56; p = 0.02) and at one month (E/A ratio: 1.2 +/- 0.7 vs 0.9 +/- 0.3; p = 0.01; EDT: 170 +/- 55 vs 207 +/- 40; p = 0.004); however no differences were observed between either group at one year in either E/A ratio (0.8 +/- 0.2 vs 0.9 +/- 0.4; NS) or EDT (207 +/- 44 vs 219 +/- 54; NS). In the large infarct group, E/A ratio decreased and EDT increased at one year compared to the first week (E/A ratio: p = 0.0004; EDT: p = 0.0001) and the first month (E/A: p = 0.02; EDT: p = 0.003); in contrast, in the small infarct group there were no significant differences in E/A ratio nor EDT during the first year postinfarction. CONCLUSIONS: In the first month postinfarction, large infarcts exhibit a greater E/A ratio and shorter EDT than small infarcts. The evolution of large infarcts is characterized by an attenuation of this pattern, with a progressive reduction of E/A ratio and prolongation of EDT during the first year post-infarction.

Diastole↗
PubMed2002

Influence of left ventricular geometry on regional systolic and diastolic function in patients with essential hypertension.

OBJECTIVE: In essential hypertension, especially in concentric hypertrophy, global diastolic function is impaired. But, whether the left ventricular (LV) geometric pattern influences regional systolic and diastolic function or not, is unknown. This study was aimed to evaluate the influence of left ventricular geometric pattern on regional systolic and diastolic function in hypertensive patients. DESIGN: Ninety untreated mild to moderate hypertensive patients were studied. M-mode parameters, standard Doppler and PW tissue Doppler indices were measured. Patients were divided into four groups according to left ventricular mass index and relative wall thickness: normal geometry (n = 16), concentric remodeling (n = 16), eccentric hypertrophy (n = 32) and concentric hypertrophy (n = 26). RESULTS: Age, gender, body mass index, systolic and diastolic blood pressure were similar among groups. E/A ratio was significantly lower in the concentric hypertrophy group compared with the normal geometry group. Em velocity and Em/Am ratio in basal septum and Em velocity in basal inferior were statistically lower in the concentric hypertrophy group compared with the normal geometry group. In the concentric hypertrophy group, the number of segments with diastolic dysfunction was significantly higher compared with the normal geometry group. LV ejection fraction and regional S velocity could be compared among groups. CONCLUSION: LV regional diastolic function is being impaired in concentric hypertrophy. LV regional systolic function does not show a difference according to the LV geometric pattern.

Adult↗
PubMed1994

Serial echocardiographic assessment of left ventricular geometry and function after large myocardial infarction in the rat.

BACKGROUND: The development of heart failure after acute myocardial infarction (MI) may be related to alterations of left ventricular (LV) structure and function. Pathological LV remodeling may exacerbate systolic and diastolic dysfunction because increased cavity dimensions tend to increase LV wall stress. Unfortunately, many complicating factors have made it difficult to clearly define the time course of LV remodeling after myocardial infarction in patients, and the contribution of structural changes to altered function has not been fully explored. METHODS AND RESULTS: To determine the type, magnitude, and time course of changes in LV geometry and function, we performed transthoracic Doppler echocardiographic examinations in rats before and 1 and 6 weeks after transmural MI induced by coronary ligation. LV internal diastolic dimension was greater in infarcted than in sham-operated rats at 1 and 6 weeks after MI (9.4 +/- 0.6 versus 8.0 +/- 0.5 and 10.1 +/- 0.9 versus 8.5 +/- 0.9 mm, respectively; P < .05 compared with sham-operated rats). There was significant thinning of the infarcted anterior wall at 1 and 6 weeks (0.99 +/- 0.2 versus 1.33 +/- 0.19 and 0.96 +/- 0.22 versus 1.51 +/- 0.18 mm, P < .05), while the thickness of the noninfarcted posterior wall increased but was not different from normal growth in sham-operated rats. Six weeks after surgery, fractional shortening was impaired (11 +/- 5% versus 35 +/- 5%, P < .05), and systolic thickening of the noninfarcted posterior wall was depressed (38 +/- 9% versus 67 +/- 18%, P < .05) in infarcted rats compared with shams. These changes in structure and systolic function were accompanied by progressive alterations in LV diastolic filling. Peak early filling velocity increased at 1 and 6 weeks in MI rats (91 +/- 9 versus 79 +/- 9 and 100 +/- 14 versus 74 +/- 11 cm/s, P < .05), and the deceleration rate of the early filling wave was more rapid in rats with MI (21.6 +/- 5.0 versus 15.6 +/- 3.1 and 26.1 +/- 9.8 versus 11.2 +/- 2.7 m/s2, P < .05). Late filling velocity was decreased (16 +/- 15 versus 33 +/- 7 and 15 +/- 18 versus 34 +/- 5 cm/s, P < .05), resulting in a marked increase in the ratio of early to late filling. The peak velocity and the velocity-time integral of LV outflow did not change after MI. CONCLUSIONS: Postinfarction LV remodeling in the rat is characterized by progressive cavity dilatation, inadequate hypertrophy of the surviving myocardium, the gradual development of regional contractile dysfunction in noninfarcted segments, and marked abnormalities of diastolic filling. These changes can be tracked longitudinally with transthoracic echocardiography.

Animals↗
PubMed1990

Effects of preload reduction on mitral flow velocity pattern in normal subjects.

In the last few years, alterations in transmitral diastolic flow pattern have been used to assess changes in left ventricular diastolic properties. However, since diastolic flow primarily reflects the atrioventricular pressure gradient, loading conditions, as well as intrinsic left ventricular properties, should be able to affect this pattern. This study was selectively designed to decrease preload (a major determinant of the atrioventricular pressure gradient) in normal subjects to observe the effects on the Doppler transmitral flow pattern without pharmacologic interventions that may also affect left ventricular diastolic properties. In 12 normal subjects, preload was reduced by inflation of blood pressure cuffs placed at the level of the root of the 4 limbs. The peak velocity of early mitral flow (E wave) decreased from 62 +/- 8 to 51 +/- 7 cm/s (p less than 0.001), while no changes were found in the maximal velocity after atrial contraction; this caused a significant decrease in the ratio of these 2 velocities (the E to A ratio) from 1.5 +/- 0.3 to 1.1 +/- 0.1 (p less than 0.001). The time-velocity integral of early diastolic inflow decreased from 7.8 +/- 1.3 to 6.1 +/- 1.3 cm (p less than 0.001) with no significant changes of the time-velocity integral of inflow after atrial contraction. Therefore, preload reduction in normal subjects significantly reduces transmitral flow in early diastole with preserved late ventricular filling, producing a pattern that can mimic the changes previously described in left ventricular diastolic dysfunction.

Adult↗
PubMed1995

Platelet-activating factor (PAF) does not affect diastolic function in isolated rat hearts.

Platelet-activating factor might be responsible for the alterations of diastolic function observed in different disease states and these potential effects have not been studied. The effect of incremental concentrations of platelet-activating factor (to a maximum of 200 nM) was therefore examined in isolated perfused rat heart. Platelet-activating factor decreased coronary flow rate and contractility in a dose-dependent manner. Although high-dose platelet-activating factor decreased peak -dP/dt compared to baseline, this was not significant when compared to vehicle-administered control. There were no changes in the time constant of left ventricular relaxation and the chamber stiffness constant. These results do not support a major direct role of platelet-activating factor in diastolic dysfunction.

Animals↗
PubMed1999

[Congestive heart failure in the aged. Causes and mechanisms of left ventricular dysfunction].

UNLABELLED: AGING PROCESS: Aging can be defined as an association of senescence and disease states. Aging induces changes in adaptive processes, modifying heart failure pathophysiology. MECHANISMS: In a population over 75, half of the patients with congestive heart failure have normal left ventricular systolic function. Heart failure in these patients results from ventricular diastolic dysfunction. Hypertension and coronary heart disease are the main causes of heart failure. THERAPEUTIC IMPLICATIONS: Identifying the etiology and the underlying mechanism (systolic or diastolic) are essential steps guiding further management.

Aged↗
PubMed1993

Does the myocardium become "stunned" after episodes of angina at rest, angina on effort, and coronary angioplasty?

To assess whether myocardial stunning occurs after brief periods of ischemia, global and regional ventricular function assessed by radionuclide angiography was studied in 52 patients. Patients were divided into 3 groups according to the type of ischemic episodes. Group 1 consisted of 15 patients studied before, during and after episodes of angina at rest. Seventeen patients studied immediately before and after coronary angioplasty constituted group 2. Group 3 consisted of 20 patients with stable angina studied before, during and after exercise-induced ischemia. Medical therapy was discontinued 48 hours before the study in all patients except those undergoing coronary angioplasty who were receiving diltiazem 180 mg/day. No difference in baseline ejection fraction was found between groups, whereas peak filling rate was statistically lower in group 3 patients. Evidence of left ventricular dysfunction during ischemia was seen in patients in groups 1 and 3, whereas transient ischemia was documented by ST-segment displacement and/or typical chest pain during balloon inflation in group 2. Persistence of systolic or diastolic dysfunction was not observed in any of the 3 groups in the recovery phase after ischemia. In conclusion, transient ischemia caused either by a primary reduction in oxygen supply (angina at rest, coronary angioplasty) or by an increase in oxygen demand (angina on effort) did not reproduce the phenomenon of systolic and diastolic stunning observed in animal experiments, although in all patients the ischemia was of sufficient duration and severity to induce marked ventricular dysfunction. The search for stunned myocardium should be extended to other different clinical models characterized by prolonged ischemia such as unstable angina or myocardial infarction.

Aged↗
PubMed1990

Determinants of hemodynamic compromise with severe right ventricular infarction.

To elucidate determinants of hemodynamic compromise in patients with acute right ventricular (RV) infarction, we studied 16 patients with hemodynamically severe RV infarction by right heart catheterization and two-dimensional ultrasound. Severe RV systolic dysfunction, evident by ultrasound in all patients as RV dilatation and depressed RV free wall motion, was associated with a broad sluggish RV waveform, diminished peak RV systolic pressure (27.6 +/- 4.5 mm Hg), and depressed RV stroke work (4.6 +/- 2.4 g.m/m2). Paradoxical septal motion was consistently noted. In some cases, the septum bulged into the right ventricle in a pistonlike fashion and appeared to mediate systolic ventricular interaction through which left ventricular septal contraction contributed to RV pressure generation. RV diastolic dysfunction was indicated by elevated RV end-diastolic pressures (13.7 +/- 2.7 mm Hg), RV "dip and plateau," equalization of diastolic filling pressures, and reversal of diastolic septal curvature toward the volume-deprived left ventricle. A prominent right atrial (RA) X and blunted Y descent, indicative of impairment of RV filling throughout diastole, were confirmed in all patients by their relation to RV systolic events. Patients manifested one of two distinct RA waveform morphologies differentiated by A wave amplitude and associated with disparate clinical courses. In eight patients, an RA W pattern was evident, characterized by augmented A waves; eight others manifested an M pattern constituted by depressed A waves. Compared with those with an M pattern, patients with a W pattern had higher peak RV pressures (29.6 +/- 3.8 versus 25.5 +/- 4.3 mm Hg, p less than 0.05), better cardiac output (3.4 +/- 0.3 versus 2.9 +/- 0.7 l/min, p less than 0.05), more favorable response to volume and inotropes, and less frequently required emergency revascularization for refractory shock (none versus five for those with an M pattern). Patients with a W pattern were more severely compromised if atrioventricular dyssynchrony developed and were more dramatically improved by restoration of physiological rhythm. Angiography in patients with depressed A waves demonstrated more proximal coronary obstruction leading to ischemic compromise of RA function, whereas in those with augmented A waves, the culprit lesion was proximal to the RV but distal to the RA branches. These results indicate that hemodynamic compromise in patients with RV infarction is exacerbated by decreased preload reserve that is dependent on atrial systole. The amplitude of the RA A wave, an indication of the status of RA function, is an important determinant of RV performance and hemodynamic compromise.

Blood Pressure↗
PubMed2003

Dynamic regulation of sodium/calcium exchange function in human heart failure.

BACKGROUND: Sarcolemmal Na/Ca exchange (NCX) regulates cardiac Ca and contractility. NCX function during the cardiac cycle is determined by intracellular [Ca] and [Na] ([Ca]i, and [Na]i) and membrane potential (Em), which all change in human heart failure (HF). Therefore, changes in NCX function may contribute to abnormal Ca regulation in human HF. METHODS AND RESULTS: We assessed the cellular bases of differences in NCX function in ventricular myocytes from failing (F) and nonfailing (NF) human hearts. Allosteric activation of NCX by [Ca]i was comparable in F and NF myocytes (K1/2=150+/-31 nmol/L, n=7). The steady-state relation between [Ca]i and NCX current (INCX) was used to infer the local submembrane [Ca]i ([Ca]sm) that is sensed by NCX dynamically during the action potential (AP) and Ca transient (37 degrees C). This involved "tail" INCX measurement during abrupt repolarization of APs and Ca transients, where peak inward INCX indicates [Ca]sm. This allows inference of the direction of Ca transport by the NCX during the AP. In NF myocytes, NCX extrudes Ca for most of the AP. Three factors shift the direction of NCX-mediated Ca transport (to favor more Ca influx) in F versus NF myocytes, as follows: (1) reduced [Ca]sm, (2) prolonged AP duration, and (3) elevated [Na]i. CONCLUSIONS: These results show that Ca entry through NCX may limit systolic dysfunction due to reduced sarcoplasmic reticulum Ca stores in HF but could contribute to slow decay of the [Ca]i transient and to diastolic dysfunction.

Action Potentials↗
PubMedDate not supplied

Correlation between left ventricular diastolic function and exercise testing in patients with old myocardial infarction.

There is no correlation between left ventricular (LV) systolic function and effort capacity of the patients with acute or old myocardial infarction (MI). On the other hand, some recent studies suggest such a relationship for LV diastolic function. Twenty-five patients with old MI were submitted to a maximal symptoms limited exercise testing (ET) and to an echo Doppler examination; functional aerobic impairment (FAI), myocardial aerobic impairment (MAI), maximal exercise capacity (METs NYHA class), isovolumic relaxation time (IVRT), E and A wave velocity, E/A rate being calculated. There is a negative significant correlation between MAI and E velocity (r = -0.68), but not between MAI and A velocity or IVRT. The data sustained the correlation between LV diastolic dysfunction and myocardial ischemia, but not with effort capacity of the patients, the last one being determined mainly by other factors. The LV diastolic function indices were modified in anterior but not in inferior MI, in relation with the amount of myocardial necrosis. It is concluded that, like LV systolic function, LV diastolic function does not correlate with the effort capacity of the patients with MI, but it represents a good predictor of the severity of myocardial ischemia mainly in anterior MI.

Diastole↗
PubMedDate not supplied

[Interconnection between segmentary contractility and dysfunction of left ventricle in patients with post-infarct cardiosclerosis ].

Intracardiac hemodynamics and segmental contractility were studied in 227 patients with postinfarction cardiosclerosis without ischemic cardiomyopathy and chronic aneurysm. Decreased ejection fraction (EF < 50%) was noted in 41 (18.1%) patients. Systolic dysfunction was frequently observed in patients with the local contractility index (LCI) exceeding 1.25. The highest degree of the left ventricular end-diastolic diameter (EDD) and end-diastolic volume (EDV) was evidenced by the anteroseptal localization of the postinfarction scar. The diastolic dysfunction of the left ventricle was mostly observed in patients with LCI less than 1.25 and posterolateral localization of scar.

Adult↗
PubMed2003

Diastolic heart failure: old story, new concepts.

Diastolic heart failure refers to a clinical syndrome characterised by symptoms and signs of congestive heart failure, with a normal or subnormal left ventricular (LV) systolic function associated with alterations in LV diastolic function. Diastolic dysfunction is a pathological condition during which the LV is unable to accept a volume of blood coming back from the lungs appropriate to maintain its stroke volume under normal filling pressure. Three eventually associated mechanisms are responsible for such dysfunction: impaired LV relaxation, increased LV stiffness and loss of normal atrial function. Prevention of LV hypertrophic remodelling should decrease the incidence of diastolic heart failure.

Heart Failure↗
PubMed2005

[Functional features of acute non-Q-wave myocardial infarction and the influence of pre-hospital treatment with propranalol, heparin and aspirin on the prognosis of the disease].

193 patients with their first non-Q-wave myocardial infarction (NQMI) were examined with the aim of studying the functional features of NQMI and estimate the influence of pre-hospital treatment with propranalol (PP), heparin and aspirin. The study found that patients having NQMI with initial ST segment depression, unlike those with initial ST segment elevation, were characterized by diffuse coronary atherosclerosis, evident diastolic dysfunction and left ventricle (LV) remodeling, progressing with the course of time. Early administration of aspirin, heparin and PP reduced LV remodeling, improved diastolic function and prognosis in patients having NQMI with initial ST segment depression.

Adrenergic beta-Antagonists↗
PubMed1992

The magnitude of left ventricular myocardial hypertrophy related to the degree of its dysfunction in patients with dilated cardiomyopathy (DCM).

The aim of the study was to analyze the relationship between the magnitude of left ventricular (LV) hypertrophy and selected haemodynamic parameters reflecting LV systolic and diastolic function. The "hypertrophy-function" relationship was evaluated in 22 patients with dilated cardiomyopathy (DCM) and in patients with left ventricular dilatation resulting from volume overload due to valve disease (DVOL). The parametres of systolic and diastolic left ventricular function were obtained from right- and left-heart catheterization and quantitative angiocardiography, DCM patients were divided into subgroups depending on the magnitude of hypertrophy and degree of dilatation: Ia- moderate hypertrophy (100 g/m2 < LVMI < 175 g/m2). Ib- massive hypertrophy (LVMI > 175 g/m2); IIa- mass/volume ratio (M/V) < 1.1, and IIb - M/V > 1.1. It was found that the magnitude of myocardial hypertrophy and the M/V ratio do not affect the degree of systolic and diastolic dysfunction in patients with DCM. Myocardial hypertrophy accompanying dilatation due to DCM and DVOL showed very similar progression of impairment of isovolumetric systole and relaxation. Significant differences in EF, LVMDP and LVEDP may result from a different degree of total LV volume stiffness as a consequence of various mechanisms of hypertrophy in DCM and DVOL.

Adolescent↗