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PubMed1998

[The echocardiographic examination in adult cardiomyopathy].

Echocardiography allows distinction between the diastolic dysfunction of hypertrophic or restrictive cardiomyopathies and the systolic dysfunction of dilated cardiomyopathy. The diagnosis and prognosis may be deduced from echocardiographic parameters. In hypertrophic cardiomyopathy systolic function is normal and there is asymmetric left ventricular hypertrophy (> 13 mm) associated with a reduced diastolic dimension and atrial dilatation resulting from diastolic dysfunction. The prognosis could be related to the severity of left ventricular hypertrophy; right ventricular hypertrophy is uncommon and its severity seems to be related to that of left ventricular hypertrophy. Restrictive cardiomyopathies are less common and amyloidosis is the commonest cause. Symmetric hypertrophy with reduced diastolic dimensions is observed; right ventricular involvement occurs in about 30% of cases. The prognosis seems to be related to the degree of parietal infiltration and, at advanced stages, systolic function is abnormal (fractional shortening < 20% with a left ventricular diastolic dimension > or = 55 mm) and rapidly fatal. Dilated cardiomyopathy is diagnosed when wall thickness is normal but left ventricular diastolic dimensions > 27 mm/m2 and ejection fraction < 45%. Right and left ventricular dimensions of the same size, left ventricular diastolic dimensions > 70 mm and left ventricular ejection fractions < 20% are poor prognostic indicators.

Adult↗
PubMedDate not supplied

Myofibril MgATPase activities and energy metabolism in cardiomyopathic mice with diastolic dysfunction.

To study the genomic physiology of cardiac myofibril proteins in the heart, we have successfully created a cardiac troponin I (cTnI; a myofibril protein) gene knockout mouse model using gene targeting techniques. The phenotype of the cTnI gene knockout mouse is a cardiomyopathy with diastolic dysfunction resulting in sudden death in neonates. In the present studies, energy metabolism was analyzed in myocardial cells from cTnI-null hearts. Myofibril MgATPase activities were determined in myocardial cells from either wild-type or cTnI mutant mouse hearts. Furthermore, the quantity and quality of the mitochondria in wild-type and cTnI mutant animals were counted and analyzed. Our results demonstrate that damaged relaxation and increased Ca(2+)-independent force production in cTnI-null hearts is in part related to the increased myofibril MgATPase activities accompanied by an increase in mitochondria quantity and mitochondrial ATPase activities. These data indicate that cardiomyopathies with diastolic dysfunction are different from cardiomyopathies caused by systolic dysfunction. The former involves the damage of cardiac relaxation due to increased MgATPase activities and increased Ca(2+)-independent force production inside of myofilaments, while the latter involves the damage of systolic contraction due to decreased MgATPase activities and decreased force production.

Animals↗
PubMed1986

Left ventricular dysfunction in patients with angina pectoris and normal coronary angiograms.

Left ventricular function was assessed in 201 patients who presented with angina pectoris and who were subsequently found to have completely normal coronary angiograms. Left ventricular angiograms from 187 patients were suitable for analysis of systolic regional wall motion; 121 were found to be normal and 66 had a total of 115 hypokinetic segments. Patients with hypokinesia had a significantly higher left ventricular end systolic volume and a significantly lower left ventricular ejection fraction and exercise capacity than those in whom regional wall motion was normal. Thirty one per cent of patients with normal wall motion and 30% of those with hypokinesia had a resting left ventricular end diastolic pressure greater than 15 mm Hg. There were significantly more smokers in the group with hypokinetic segments. Thus of patients with angina and normal coronary angiograms, 25% had evidence of left ventricular systolic dysfunction, 20% had evidence of diastolic dysfunction, and 11% had evidence of both systolic and diastolic dysfunction. The results suggest that smoking may be associated with left ventricular regional wall motion abnormalities.

Adult↗
PubMed2002

Cardiac effects of low-dose growth hormone replacement therapy in growth hormone-deficient adults. An 18-month randomised, placebo-controlled, double-blind study.

OBJECTIVE: To characterise the effect of long-term low-dose growth hormone (GH) treatment on cardiac anatomy and function. METHODS: 20 patients with multiple pituitary hormone deficiencies, including severe acquired GH deficiency (GHD), were randomly assigned to GH or placebo (P) for 18 months. Echocardiographic measurements were performed at baseline and after 6, 12 and 18 months. RESULTS: At baseline, 8 of 20 patients had diastolic dysfunction (6 severe and 2 borderline), while only 1 had systolic dysfunction. None of the investigated parameters of diastolic or systolic function changed during treatment. CONCLUSION: In adult onset GHD, diastolic dysfunction was present in 40% of the patients. None of the investigated values were different after 18 months of GH compared to placebo.

Adenoma↗
PubMed1996

Congestive heart failure with normal left ventricular systolic function. Clinical approaches to the diagnosis and treatment of diastolic heart failure.

The syndrome of congestive heart failure with preserved left ventricular systolic function is common in clinical practice. The signs and symptoms of the disorder are similar to those of congestive heart failure with left ventricular systolic dysfunction, underscoring a need for routine evaluation of left and right ventricular systolic function in patients with congestive heart failure. The syndrome may be related to anatomic abnormalities that increase the resistance to ventricular filling, or to physiologic abnormalities of myocardial relaxation or compliance. Advancing age, often in association with hypertension, coronary artery disease, tachycardia, and atrial fibrillation, is commonly associated with the disorder. Randomized controlled clinical trials are needed to evaluate the efficacy of various therapeutic agents in reducing the risks associated with diastolic heart failure.

Algorithms↗
PubMed2005

Patient selection for cardiac resynchronization therapy: from the Council on Clinical Cardiology Subcommittee on Electrocardiography and Arrhythmias and the Quality of Care and Outcomes Research Interdisciplinary Working Group, in collaboration with the Heart Rhythm Society.

Cardiac resynchronization therapy (CRT) is a relatively new therapy for patients with symptomatic heart failure resulting from systolic dysfunction. CRT is achieved by simultaneously pacing both the left and right ventricles. Biventricular pacing resynchronizes the timing of global left ventricular depolarization and improves mechanical contractility and mitral regurgitation. Published clinical trials have demonstrated that CRT results in improved clinical status and lower mortality rate when selected patients with systolic ventricular dysfunction and heart failure are treated with CRT. This advisory identifies appropriate candidates for CRT on the basis of the inclusion criteria and results from the published clinical trials.

Arrhythmias, Cardiac↗
PubMedDate not supplied

[Postoperative changes in diastolic function of the left ventricle in patients with aortic valve stenosis].

INTRODUCTION: Diastolic dysfunction in valvular aortic stenosis frequently precedes systolic dysfunction. The purpose of this study was to examine the changes in left ventricular diastolic function after aortic valve replacement. METHODS: Seventy eight patients with significant isolated valvular aortic stenosis were enrolled in the study. The echocardiographic examination was performed with ACUSON-XP 10 imaging system. Complete M-mode, 2-dimensional and Doppler echocardiographic results were obtained. In 48 patients right and left heart catheterisation was performed. Left ventricular diastolic function was evaluated by pulse Doppler recording of inflow velocity on the tips of the mitral valve leaflets. Forty two underwent aortic valve replacement. They were followed up 6-12 months postoperatively. RESULTS: Abnormal patterns of left ventricular diastolic filling were noticed in almost all patients (Table 1). Most prominent changes were found in subjects with marked and diffuse hypertrophy (Table 2). After aortic valve replacement decrease in left ventricular size, mass, pressures and improvement in systolic Function (Table 3). Twelve months after the operation late diastolic filling velocity was lower (A = 64 +/- 15 cm/s, Avti = 7.1 +/- 1.8 cm), early diastolic filling velocity was higher (E = 83 +/- 14 cm/s, Evti = 10.3 +/- 1.4 cm), deceleration time (DT = 123 +/- 14 ms) and isovolumetric relaxation time (IRT = 66 +/- 6 ms) were longer in patients with preoperative moderate hypertrophy (Table 4). In patients with severe left ventricular hypertrophy changes in diastolic function were slower. We found decrease in early diastolic filling velocity (A = 44 +/- 6 cm/s, Avti = 4.6 +/- 04 cm), increase in late diastolic filling velocity (E = 67 +/- 14 cm/s, Evti = 9.4 +/- 1.7 cm), with prolongation of deceleration (DT = 131 +/- 18 ms) and isovolumetric relaxation time (IRT = 94 +/- 23 ms) (Table 5). DISCUSSION: In adults with significant sympthomatic aortic valve stenosis, aortic valve replacement is therapy of choice. Replacement of the diseased aortic valve with a prosthetic valve yields relief of left ventricular outflow obstruction. Myocardial remodeling with regression of mass transpires as the heart adapts to the new level of afterload. In patients with moderate left ventricular hypertrophy improvement in diastolic function during the first year after aortic valve replacement is visible, while in patients with extreme myocardial hypertrophic changes it was slower.

Adolescent↗
PubMed1999

Natriuretic peptides in patients with diastolic dysfunction due to idiopathic dilated cardiomyopathy.

AIMS: The degree of systolic dysfunction does not always correlate with functional impairment in patients with congestive heart failure. In contrast, diastolic dysfunction correlates well with functional impairment. In heart failure, both elevation of N-terminal proatrial natriuretic peptide and B-type natriuretic peptide are markers of a poor prognosis. METHODS: We investigated 32 patients (26 male, 6 female; mean age 55+/-2 years) with dilated cardiomyopathy and sinus rhythm. M-mode echocardiography and 2D-echocardiography were carried out in each patient. Pulsed-wave Doppler inflow signals were obtained and the following parameters were measured: maximal E wave and maximal A wave velocity, E/A ratio, E wave deceleration time, A wave deceleration time. Immediately after echocardiography blood samples were collected from patients in the supine position. N-terminal proANP and brain natriuretic peptide were measured using a radioimmuno assay. RESULTS: The left ventricular ejection fraction was 34+/-1%, the left ventricular end-diastolic diameter on M-mode echocardiography was 68+/-1 mm, while left atrial diameter was 45+/-1 mm. Univariate analysis revealed a significant correlation between both left atrial diameter and ejection fraction and N-terminal proANP and brain natriuretic peptide. All transmitral Doppler parameters showed a significant correlation with N-terminal proANP and brain natriuretic peptide. On forward stepwise regression analysis, left atrial diameter and ejection fraction were able to predict both N-terminal proANP and brain natriuretic peptide. However, of the diastolic parameters only the E/A ratio remained significant. Mildly symptomatic patients differed significantly from severely symptomatic patients in all Doppler parameters. Mildly symptomatic patients had significantly lower levels of N-terminal proANP (0.571+/-0.079 vs 2.282+/-0.340 nmol. l(-1);P<0.001) and brain natriuretic peptide (51+/-14.8 vs 474.2+/- 86.8 pg. ml(-1);P<0. 001). CONCLUSION: There is a close relationship between natriuretic peptides and diastolic Doppler parameters of left ventricular filling in patients with dilated cardiomyopathy. There is also a significant difference between patients with mild and severe functional impairment regarding both natriuretic peptides and transmitral Doppler parameters.

Atrial Natriuretic Factor↗
PubMed2000

Clinical profile and outcome of idiopathic restrictive cardiomyopathy.

BACKGROUND: Idiopathic restrictive cardiomyopathy is a poorly recognized entity of unknown cause characterized by nondilated, nonhypertrophied ventricles with diastolic dysfunction resulting in dilated atria and variable systolic function. METHODS AND RESULTS: Between 1979 and 1996, 94 patients (61% women) 10 to 90 years old (mean, 64 years) met strict morphological echocardiographic criteria for idiopathic restrictive cardiomyopathy, mainly dilated atria with nonhypertrophied, nondilated ventricles. None had known infiltrative disease, hypertension of >5 years' duration, or cardiac or systemic conditions associated with restrictive filling. Nineteen percent were in NYHA class I, 53% in class II, and 28% in class III or IV. Atrial fibrillation was noted in 74% of patients and systolic dysfunction in 16%. Follow-up (mean, 68 months) was complete for 93 patients (99%). At follow-up, 47 patients (50%) had died, 32 (68%) of cardiovascular causes. Four had heart transplantation. The death rate compared with actuarial statistics was significantly higher than expected (P<0.0001). Kaplan-Meier 5-year survival was 64%, compared with expected survival of 85%. Multivariate analysis using proportional hazards showed that the risk of death approximately doubles with male sex (hazard ratio [HR] = 2.1), left atrial dimension >60 mm (HR = 2.3), age >70 years (HR = 2.0), and each increment of NYHA class (HR = 2.0). CONCLUSIONS: Idiopathic restrictive cardiomyopathy or nondilated, nonhypertrophic ventricles with marked biatrial dilatation, as defined morphologically by echocardiography, affects predominantly elderly patients but can occur in any age group. Patients present with systemic and pulmonary venous congestion and atrial fibrillation and have a poor prognosis, particularly men >70 years old with higher NYHA class and left atrial dimension >60 mm.

Adolescent↗
PubMed1995

Exercise training improves left ventricular diastolic filling in patients with dilated cardiomyopathy. Clinical and prognostic implications.

BACKGROUND: Patients with dilated cardiomyopathy (DCM) often have left ventricular (LV) diastolic dysfunction that can precede the development of systolic dysfunction. Recent reports showed that exercise training (ET) improves the exercise capacity of these patients. Although this improvement is primarily due to peripheral adaptations, the contribution of LV diastolic filling has not been well defined. The purpose of this study was to determine whether ET can induce changes in LV diastolic filling that can account for an increase in exercise capacity and whether these changes can influence prognosis. METHODS AND RESULTS: We prospectively studied 55 consecutive patients (mean age, 55 +/- 7 years) with DCM. Patients were randomized into a training group (36 patients) or a control untrained group (19 patients) and matched for clinical and functional characteristics. All patients underwent a pulsed Doppler echocardiographic study, a radionuclide angiographic study, and a cardiopulmonary exercise test before and after a 2-month ET program. On the basis of the Doppler LV diastolic filling pattern at the beginning of the study, patients were prospectively divided into three subgroups: A (restrictive pattern), B ("normal" pattern), and C (abnormal relaxation pattern). In the trained group, peak VO2 (+12%; P < .0001), peak workload (+8.5%; P < .005), and lactic acidosis threshold (+12%; P < .0001) were significantly increased after training without changes in LV ejection fraction. However, only subgroup C demonstrated significant improvement in peak VO2 (+15%; P < .005). No changes were observed in the untrained group. In the trained subgroups a significant increase in rapid filling fraction (RFF), peak filling rate (PFR), peak early filling velocity (E), and E/A ratio was noted. A significant decrease in atrial filling fraction (AFF), peak atrial filling velocity (A), deceleration time of early filling velocity (EDT), and isovolumic relaxation time (IVRT) was observed only in subgroup C. No changes were found in untrained subgroups. A good correlation was found between Doppler and radionuclide LV diastolic filling parameters before and after training (P < .0001). Multiple stepwise regression analysis demonstrated that pretraining E/A ratio (P < .0001) and peak heart rate (P < .0002) were positive predictors of pretraining peak VO2. Posttraining increase in exercise tolerance (P < .0001) and increase in E/A ratio (P < .0001) were the strongest predictors of an increase in peak VO2. The independent predictors of cardiac events were a greater RFF and a shorter IVRT and EDT. Stepwise logistic regression showed that Doppler LV diastolic filling patterns are independent predictors of overall cardiac events (P = .02), and restrictive pattern has a worse prognosis compared with B (P = .04) and C (P = .007). However, ET did not reach statistical significance (P = .54) as a predictor of cardiac events. CONCLUSIONS: These data demonstrate that ET induces significant improvement in exercise capacity only in patients with DCM and a pattern of abnormal LV relaxation. The improvement in peak VO2 is significantly correlated with an increase in peak early filling rate and peak filling rate as well as a decrease in atrial filling rate. Doppler echocardiography may be a valuable tool in the prognostic assessment of patients with DCM who will benefit from exercise training.

Blood Flow Velocity↗
PubMed2006

Epinephrine increases mortality after brief asphyxial cardiac arrest in an in vivo rat model.

Epinephrine may be detrimental in cardiac arrest. In this laboratory study we sought to characterize the effect of epinephrine and concomitant calcium channel blockade on postresuscitation myocardial performance after brief asphyxial cardiac arrest. Anesthesized rats were disconnected from mechanical ventilation, resulting in cardiac arrest. Resuscitation was attempted after 1 min with mechanical ventilation, oxygen, chest compressions, and IV medication. In experimental series 1 and 2, animals were allocated to 10 or 30 microg/kg epinephrine or 0.9% saline. In series 3, animals received 30 microg/kg of epinephrine and were randomized to 0.1 mg/kg of verapamil or to 0.9% saline. In series 1 and 3, left ventricular function was assessed using transthoracic echocardiography. In series 2, left atrial pressure was measured. Epinephrine was associated with increased mortality (0/8 [0%] in controls, 4/12 [33.3%] in 10 microg/kg animals, and 16/22 [72.8%] in 30 microg/kg animals; P < 0.05), hypertension (P < 0.001), tachycardia (P = 0.004), early transient left atrial hypertension, and dose-related reduction in left ventricular end diastolic diameter (P < 0.05). Verapamil prevented mortality associated with large-dose epinephrine (0% versus 100%) and attenuated early diastolic dysfunction and postresuscitation hypertension (P = 0.001) without systolic dysfunction. Epinephrine appears to be harmful in the setting of brief cardiac arrest after asphyxia.

Animals↗
PubMed2000

[Hospital readmission for heart failure in a general hospital].

OBJECTIVE: Heart failure (HF) is the most common discharge diagnosis for admission and readmission in adult. Prior studies have reported that elderly patients who survive hospitalization for HF, are particularly vulnerable to readmission. The present study was realized to investigate the characteristics of patients with readmissions for HF and the features of this hospitalizations. METHODS: This observational study, looked for patients with two or more hospital admissions with diagnosis of HF in 1996 in Gregorio Marañón General Hospital (Madrid). From them, it was taken a random sample. Second and following admissions were studied (readmission). RESULTS: There were 1561 hospitalizations for HF in 1996, being 349 second or following admissions (22.4%). After analyzing 153, it was found a 75.8% of readmissions in the first 90 days after discharge. The mean age was 77.4 +/- 10.31. More than a half were women and patients have an important comorbidity (pathologies presented more frequently were Diabetes Mellitus and airways obstructive diseases). From patients with echocardiography performed before readmission, 66.4% present left ventricular systolic dysfunction and 33.6% have normal left ventricular systolic function. The principal aetiologies were coronary artery disease, valvular heart disease and hypertension (in those patients in which aetiology have been investigated). CONCLUSION: Readmission after a hospitalization for HF is common, with a high percentage of patients readmitted in a short time. This rate demands efforts to identify patients with a higher likelihood of readmission and develop programs to clarify the determinants of this problem and thus improve it.

Aged↗
PubMed2000

[Idiopathic cardiomyopathy: pathophysiology and hemodynamics].

Idiopathic cardiomyopathy is classified into three categories, namely, hypertrophic, dilated and restrictive cardiomyopathy. Pathophysiology and hemodynamics are quite different between the three types of cardiomyopathies. Hypertrophic cardiomyopathy is hemodynamically characterized by outflow obstruction and diastolic dysfunction. In dilated cardiomyopathy, progressive dilatation and systolic dysfunction of the left ventricle are predominant. This left ventricular remodeling is strongly associated with neurohormonal activation occurred in this disease. In restrictive cardiomyopathy, left ventricular distensibility is markedly impaired and differential diagnosis from constrictive pericarditis is often difficult.

Cardiomyopathies↗
PubMed2006

[Early diagnosis of pulmonary hemodynamic disorders in patients with pulmonary sarcoidosis].

A hundred and eleven patients with pulmonary sarcoidosis (PS) were examined to detect early impairments of pulmonary hemodynamics and myocardial function. A package of examinations included Doppler echocardiography at rest and with the Valsalva test, as well as electrocardiography and myocardial scintigraphy. In patients with early PS, right ventricular diastolic dysfunction is shown to be preceded by systolic dysfunction, as manifested itself in the altered ratio of different phases of right ventricular filling. As a method for early diagnosis of latent hypertension, the authors propose to use the Valsalva test to create a short-term volume overload of the right cardiac cavities. The study has indicated that left cardiac dilatation, decreased ejection fraction, left ventricular diastolic dysfunction, and the presence of large focal portions of fibrosis in the ventricular myocardium, interventricular septum, and papillary muscles can be considered to be early Doppler echocardiographic signs of sarcoidosis of the heart in patients with PS.

Acute Disease↗
PubMed1987

Relation between cardiac dyspnea and left ventricular function. A non-invasive study of 67-year-old men.

The relation of dyspnea of presumed cardiac origin to regional and global left ventricular (LV) function was evaluated among 67-year old men sampled from the general population of Gothenburg, Sweden. From a screened cohort of 644 men, 42 men with cardiac dyspnea and without obstructive pulmonary disease, and 45 controls were sampled. Dyspnea was measured and graded according to the World Health Organization standard. Two-dimensional and M-mode echocardiography, carotid pulse tracing, apexcardiography and phonocardiography were used to evaluate regional wall motion, systolic time intervals, LV ejection indices, wall stress, diastolic time intervals, direct and indirect indices of LV filling properties, and indices of pulmonary hypertension. The plasma concentrations of immunoreactive atrial natriuretic peptide (IrANP) and catecholamines were also assessed. The dyspneic men had more regional wall motion abnormalities than the controls. Systolic, as well as diastolic LV impairment, and increased LV mass were more abundant. Dyspnea grade was significantly related to either of these abnormalities in univariate analyses, and also in multivariate analyses when clinical information, such as chest X-ray, electrocardiogram, and clinical history were taken into account. Multivariate analyses of all the studied indices of cardiac function, together with clinical information, showed dyspnea grade to be significantly and independently related to mitral valve E-point to septal separation (EPSS), presence of akinetic segments, a history of angina pectoris, exercise capacity, and left atrial dimension. Taken together these variables explained 74% of dyspnea grade variance. There was also a relation between dyspnea grade and IrANP, which was independent of clinical findings, but only appeared under conditions of severe dyspnea. It is concluded that the degree of dyspnea is associated with a fairly similar progressive impairment of diastolic, regional and systolic function. In mild heart failure LV hypertrophy and diastolic abnormalities are more prevalent than systolic dysfunction. In severe dyspnea a mixture of regional, systolic, and diastolic abnormalities are present. A decrease of fractional shortening and increased levels of IrANP are late phenomena. EPSS may be a useful indicator of LV dysfunction in population studies.

Aged↗
PubMed2003

Effect of left ventricular function on long-term left ventricular pacing and sensing threshold.

BACKGROUND: The effect of left ventricular (LV) systolic function on the long-term left ventricular pacing and sensing threshold is unclear. METHODS AND RESULTS: We studied the effect of LV ejection fraction (LVEF) on the LV pacing and sensing threshold in 56 patients (mean age: 70.2 +/- 10.5 years) underwent permanent LV pacing using a self-retaining coronary sinus lead (Model 1055 K, St Jude Medical, USA). In 49 patients, the LV lead was implanted for conventional pacemaker indication (sick sinus syndrome = 14, heart block = 26 or slow atrial fibrillation = 9). The remaining 7 patients were implanted for congestive heart failure. The LV pacing and sensing threshold, and lead impedance were compared between patients with LVEF <40% (Group 1, n = 28) and LVEF >40% (Group 2, n = 28) during implant and at 3-month follow up. The LV pacing lead was successfully implanted in all patients without any lead dislodgement on follow-up. At implant, Group 1 patients had a significant lower R wave amplitude, but similar LV pacing threshold and lead impedance as compared to Group 2. However, at 3-month follow-up, Group 1 patients had a significantly higher LV pacing threshold compared to Group 2 patients. There were no significant differences in the sensing threshold and lead impedance between the two groups. Furthermore, there was also a significant interval increase in LV pacing threshold in Group 1 patients (0.94 +/- 0.12 V) after 3 months, but not in Group 2 patients (0.16 +/- 0.08 V, p < 0.01). CONCLUSIONS: The results of this study suggest that the LV systolic function has a significant impact on the long-term LV pacing threshold. The long-term left ventricular pacing threshold in patients with left ventricular systolic dysfunction increased after implant and was higher than patients with normal left ventricular systolic function.

Aged↗
PubMed1995

Remodelling of intramyocardial arterioles and extracellular matrix in patients with arterial hypertension and impaired coronary reserve.

The heart in pressure overload is threatened by the development of diastolic and systolic dysfunction even in the absence of coronary heart disease. In pressure overload, systolic wall stress leads to an increase in left ventricular mass through hypertrophy of myocytes. An activation of myocytic as well as non-myocytic cells is present. An increase in interstitial collagen accompanies hypertrophy of the myocytes. Thus, myocytic hypertrophy and fibrosis cause diastolic dysfunction early on, even when systolic function is still well preserved. In hypertensive heart disease, the coronary microcirculation is remodelled by thickening of the walls of intramyocardial arterioles in relation to their lumen and by an increase in periarteriolar fibrosis. This remodelling of the intramyocardial vasculature is combined with a reduction in coronary vasodilator reserve that may lead to malnutrition and malperfusion of the hypertrophied myocytes. The combined processes of myocytic hypertrophy, vascular remodelling and increased fibrosis may be important in the process of ventricular dilatation and failure in hypertensive heart disease.

Adult↗
PubMed2006

Usefulness of clinical, electrocardiographic, and echocardiographic parameters to detect cardiac asynchrony in patients with left ventricular dysfunction secondary to ischemic or nonischemic heart disease.

OBJECTIVES: Specific evaluation using echocardiographic Doppler is superior to the measurement of the QRS complex to detect cardiac asynchrony. Nevertheless, no clinical, electrocardiographic, or echocardiographic parameters have been evaluated to obtain an accurate and easy-to-use marker of cardiac asynchrony in patients with depressed left ventricular (LV) ejection fraction. Our aim was to determine whether there is any marker of cardiac asynchrony in patients with LV systolic dysfunction that allows us to obviate the performance of a specific echocardiographic study before cardiac resynchronization therapy. METHODS: In all, 316 consecutive patients with LV ejection fraction less than 40% were enrolled. Interventricular asynchrony was defined as an interventricular mechanical delay longer than 40 milliseconds. Intraventricular asynchrony was defined as the difference between time from Q wave to LV ejection end and the time from Q wave to the end of the systolic wave of the most delayed basal segment by Doppler tissue imaging greater than 50 milliseconds. RESULTS: In all, 177 (56%) had ischemic and 139 (44%) had nonischemic heart disease. The logistic regression analysis showed that only the presence of left bundle branch block was an independent predictor of interventricular asynchrony despite the cause of the underlying disease (odds ratio and 95% confidence interval 7.2 [3.9-13.4], P < .001; 5.99 [2.7-13.2], P < .001; and 8.75 [3.2-23.8], P < .001 for the total population, ischemic and nonischemic groups, respectively). Nevertheless, none of the studied parameters was found as a predictor of intraventricular asynchrony. CONCLUSIONS: The presence of left bundle branch block is a marker of interventricular asynchrony in patients with ventricular dysfunction despite the cause of the underlying cardiac disease. Nevertheless, intraventricular cardiac asynchrony cannot be detected using conventional parameters. A specific echocardiographic evaluation before cardiac resynchronization therapy must be performed in all these patients. Our aim was to determine whether there is any marker of cardiac asynchrony in patients with left ventricular systolic dysfunction that allows us to obviate the performance of a specific echocardiographic study before cardiac resynchronization therapy. Our results showed that only the presence of left bundle branch block was an independent predictor of interventricular asynchrony despite the cause of the underlying disease but none of the studied parameters was found as a predictor of intraventricular asynchrony.

Arrhythmias, Cardiac↗