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PubMed1997

Changes in right ventricular filling dynamics during left anterior descending, left circumflex and right coronary artery balloon occlusion.

AIM: Transient coronary artery occlusion during percutaneous transluminal coronary angioplasty may cause left ventricular diastolic dysfunction. The aim of this study was to evaluate the effect of left anterior descending, left circumflex and right coronary artery balloon occlusion on right ventricular diastolic function. METHODS: Thirty-five patients with single-vessel coronary artery disease and no previous myocardial infarction were selected. Left and right ventricular filling pressures were monitored by Doppler echocardiography and haemodynamic monitoring. This was performed during and immediately after 60 s of coronary balloon occlusion of the left anterior descending artery in 21 cases (Group 1), the left circumflex artery in eight cases (Group 2) and the right coronary artery in six cases (Group 3). Doppler analysis of left and right ventricular filling included peak velocity of early (PFVE) and late ventricular filling (PFVA) and PFVE to PFVA ratio (PFVE/PFVA). RESULTS: In all three groups, balloon inflation induced a significant increase in left and right filling pressures (P < 0.05). No qualitative difference in haemodynamic changes was found between groups during inflation. Significant impairment in the Doppler pattern of left and right ventricular filling occurred after 20 s of coronary occlusion: PFVE values in mitral and tricuspid valves decreased by 14% and 25% in Group 1, 13% and 25% in Group 2, and 10% and 21% in Group 3, respectively, as PFVA remained unchanged in all groups, the PFVE/PFVA ratio of mitral and tricuspid valve flows significantly decreased (Group 1: -12% and -20%, Group 2: -10% and -21%, Group 3: -14% and -21%, respectively). All parameters returned to baseline within 30 s after each balloon deflation. CONCLUSION: Our data suggest that brief episodes of acute myocardial ischaemia, such as those induced by 60 s of coronary artery occlusion during percutaneous transluminal coronary angioplasty, elicit simultaneous diastolic dysfunction of both ventricles, independent of the coronary artery involved.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

Serial echocardiography in transplanted heart: an initial report of five cases.

Role of echocardiography including Doppler is established in selection of donor and in the care of patients after cardiac transplantation. Its value for recognition of transplant rejection is however still evolving. We present here, serial echocardiographic findings in five male patients, aged 22 to 46 years who underwent cardiac transplantation at our institution. There was no appreciable change on follow-up in the left ventricular dimensions, thickness of left ventricular posterior wall and interventricular septum and left ventricular systolic function. Transient pericardial effusion was noted in two patients. Trivial to mild mitral and tricuspid regurgitation was observed. The diastolic function of the left ventricle, as assessed by mitral valve inflow wave pattern, was normal in four patients. However in the fifth patient, there was evidence of diastolic dysfunction of the left ventricle and this change was accompanied by rejection episode (IIIB changes) in the endomyocardial biopsy. With resolution of rejection in biopsy, the diastolic function by Doppler also returned to normal. We conclude that echocardiography has a definite role in the general care of patients after cardiac transplantation. Transient small pericardial effusion and mild atrioventricular valve regurgitation are common after the operation. Echocardiography may also be of use in recognition of rejection episode by demonstrating evidence of diastolic dysfunction of the left ventricle. Currently, endomyocardial biopsy remains the gold standard for diagnosis of rejection.

Adult↗
PubMed1995

Effect of age and pathology on left ventricular diastolic function: the diagnostic yield of Doppler echocardiography.

BACKGROUND: Doppler echocardiography has been proposed to detect left ventricular (LV) diastolic dysfunction in the elderly. However, the validity of this technique in differentiating the effects of pathology from those of normal aging has not been defined. METHODS: Doppler indices of LV diastolic function were obtained in 85 patients (34 hypertensive, 29 with coronary artery disease, 22 with both conditions) and in 56 healthy volunteers. RESULTS: A linear correlation with age was found for all parameters in controls, and for many parameters in patients. Also, in the presence of heart diseases, age exerted a powerful, independent effect on Doppler parameters. None of these differed between patients and controls in advanced age. CONCLUSION: Due to the prevailing age-related variations in Doppler indices of diastolic performance occurring beyond the age of 65, Doppler echocardiography cannot be employed to diagnose LV diastolic dysfunction in the elderly.

Adult↗
PubMed1993

Diastolic function in children and adolescents on dialysis and after kidney transplantation: an echocardiographic assessment.

Thirty-seven children and adolescents on renal replacement therapy (11 on haemodialysis, 14 on continuous ambulatory peritoneal dialysis and 12 after renal transplantation) were studied by echocardiography, echo-Doppler and phonocardiography. Right and left ventricular (R/L V) diastolic functions were measured by transmitral and transtricuspid flow velocities and by LV isovolumic relaxation time (LVIRT). Thirty-seven age- and sex-matched healthy subjects served as controls. R/L V diastolic dysfunction was only observed in the dialysis patients. In these patients LVIRT was prolonged. LV and RV peak inflow velocities were increased both in early (E) and late (A) diastole with a reduction in the E/A ratios. This pattern of diastolic dysfunction is compatible with the combined effects of a hypercirculatory state (volume overload, anaemia, arteriovenous fistula) and an abnormality of cardiac relaxation. The transplant patients showed no major cardiac abnormalities.

Adolescent↗
PubMed2005

Left ventricular dysfunction in patients with subclinical hypothyroidism and its reversibility after hormone therapy.

AIM: To ascertain the presence of LV dysfunction in patients of subclinical hypothyroidism and its reversibility after hormone therapy. METHODS AND METERIAL: Thirty two patients with subclinical hypothyroidism (SH) were included in the study, along with thirty two age and sex matched individuals serving as controls. The patients with SH had normal serum T3 and T4 with an elevated TSH value. All patients and the controls were subjected to detailed echocardiographic examination for assessment of LV systolic and diastolic function before and one year after hormone (thyroxine) therapy. RESULTS: The systolic function of LV was normal in patients with SH. There was significant diastolic dysfunction in the SH patients as compared with controls. There was prolongation of deceleration above time (169 +/- 6.1 msec. vs. 148.1 +/- 5.4 msec in controls, p < 0.05), isovolumic relaxation time (89.1 +/- 7.3 msec vs. 79.4 +/- 5.9 msec., p<0.05), increased A wave (0.63 +/- 0.6 m/sec. vs. 0.54 +/- 0.05 m/sec) and reduced E/A ratio (0.7 +/- 0.09 vs. 1.4 +/- 0.3, p < 0.05). Echocardiography at the end of one year of hormone therapy revealed considerable improvement in diastolic function of the LV. There was significant improvement in DT (from 169 +/- 6.1 msec. to 151 +/- 5.2 msec, p < 0.05), IVRT (from 89.1 +/- 7.3 msec. to 80.2 +/- 6.5 msec, p < 0.05) and increased E/A ratio (from 0.7 +/- 0.09 to 1.3 +/- 0.1, p < 0.05). CONCLUSION: Hypothyroidism, even in subclinical stage, can cause diastolic dysfunction of the LV. These abnormalities in diastolic function can be reversed by thyroxine therapy.

Adult↗
PubMed2003

Preload dependence of new Doppler techniques limits their utility for left ventricular diastolic function assessment in hemodialysis patients.

Left ventricular (LV) hypertrophy leads to diastolic dysfunction. Standard Doppler transmitral and pulmonary vein (PV) flow velocity measurements are preload dependent. New techniques such as mitral annulus velocity by Doppler tissue imaging (DTI) and LV inflow propagation velocity measured from color M-mode have been proposed as relatively preload-independent measurements of diastolic function. These parameters were studied before and after hemodialysis (HD) with ultrafiltration to test their potential advantage for LV diastolic function assessment in HD patients. Ten patients (seven with LV hypertrophy) underwent Doppler echocardiography 1 h before, 1 h after, and 1 d after HD. Early (E) and atrial (A) peak transmitral flow velocities, peak PV systolic (s) and diastolic (d) flow velocities, peak e and a mitral annulus velocities in DTI, and early diastolic LV flow propagation velocity (V(p)) were measured. In all patients, the E/A ratio after HD (0.54; 0.37 to 1.02) was lower (P < 0.01) than before HD (0.77; 0.60 to 1.34). E decreased (P < 0.01), whereas A did not. PV s/d after HD (2.15; 1.08 to 3.90) was higher (P < 0.01) than before HD (1.80; 1.25 to 2.68). Tissue e/a after HD (0.40; 0.26 to 0.96) was lower (P < 0.01) than before HD (0.56; 0.40 to 1.05). Tissue e decreased (P < 0.02), whereas a did not. V(p) after HD (30 cm/s; 16 to 47 cm/s) was lower (P < 0.01) than before HD (45 cm/s; 32 to 60 cm/s). Twenty-four hours after the initial measurements values for E/A (0.59; 0.37 to 1.23), PV s/d (1.85; 1.07 to 3.38), e/a (0.41; 0.27 to 1.06), and V(p) (28 cm/s; 23 to 33 cm/s) were similar as those taken 1 h after HD. It is concluded that, even when using the newer Doppler techniques DTI and color M-mode, pseudonormalization, which was due to volume overload before HD, resulted in underestimation of the degree of diastolic dysfunction. Therefore, the advantage of these techniques over conventional parameters for the assessment of LV diastolic function in HD patients is limited. Assessment of LV diastolic function should not be performed shortly before HD, and its time relation to HD is essential.

Adult↗
PubMed2004

Left ventricular dysfunction in normotensive Type 1 diabetic patients: the impact of autonomic neuropathy.

AIMS: The pathophysiological mechanisms responsible for increased cardiovascular mortality in diabetic autonomic neuropathy (AN) are largely unknown. The aim was to determine the relative role of AN in the pathogenesis of cardiac diastolic dysfunction and left ventricular hypertrophy in Type 1 diabetes. METHODS: Ten Type 1 diabetic patients with AN, defined by cardiovascular tests (AN+) and 10 age- and sex-matched patients without neuropathy (AN-) as well as 10 healthy subjects (C) participated in the study. Left ventricular diastolic function was assessed by Doppler echocardiography, whilst systolic function was evaluated by cine magnetic resonance (MR) imaging. RESULTS: Doppler echocardiography showed a significant decrease in E/A ratio, i.e. the ratio between peak Early transmitral filling velocity during early diastole (E-wave) and peak transmitral Atrial filling velocity during late diastole (A-wave), in AN+ compared with C (P < 0.01) [0.95 +/- 0.08 (mean +/- sem) (AN+); 1.19 +/- 0.09 (AN-); 1.33 +/- 0.10 (C)]. The E-wave deceleration time was significantly shorter in AN+ compared with AN- and C (P < 0.02) [178 +/- 7 ms (AN+); 203 +/- 9 ms (AN-); 205 +/- 9 ms (C)]. Cine MR imaging showed a significantly greater left ventricular mass index in AN+ compared with C [103 +/- 4 g/m(2) (AN+) vs. 98 +/- 7 (AN-) and 92 +/- 4 g/m(2) (C), P < 0.05]. CONCLUSION: Autonomic neuropathy is associated with left ventricular hypertrophy and diastolic dysfunction in Type 1 diabetic patients.

Autonomic Nervous System Diseases↗
PubMed1994

The ever expanding spectrum of ischemic left ventricular dysfunction.

Ischemic left ventricular (LV) dysfunction includes a number of discrete entities, such as acute LV failure in angina, acute myocardial infarction, and ischemic cardiomyopathy. Recently, new entities have arisen to expand the spectrum of ischemic LV function. These include postinfarct diastolic dysfunction, stunning, hibernation, and preconditioning. The tantalizing possibility exists that several of these states can coexist. There are widely differing underlying pathophysiologic states. Hence it is not easy to be dogmatic about whether a given group of therapeutic agents, such as the calcium antagonists, may be beneficial in ischemic LV dysfunction. Nonetheless, there is experimental evidence that calcium antagonists may benefit the specific entity of stunning and clinical evidence that they benefit postinfarct ischemic LV diastolic dysfunction. These agents, as a group, should be evaluated in reperfusion and postinfarct dysfunctional syndromes.

Acute Disease↗
PubMed2006

Diastolic heart failure in the elderly and the potential role of aldosterone antagonists.

The overall incidence of heart failure increases with age, affecting up to 10% of people >65 years of age. Diastolic heart failure is also age-dependent, increasing from <15% in middle-aged patients to >40% in patients > or =70 years of age. Elderly patients usually have other co-morbid conditions such as hypertension, diabetes mellitus, coronary artery disease and atrial fibrillation that can adversely affect the diastolic properties of the heart. The clinical manifestations of diastolic heart failure are similar to those of systolic heart failure. In practice, the diagnosis is generally based on the finding of typical symptoms and signs of heart failure with preserved left ventricular ejection fraction and no valvular abnormalities on echocardiography. Altered ventricular relaxation and abnormal ventricular filling are the hallmarks of diastolic heart failure. Cardiac fibrosis and cellular disarray lead to the alterations in the diastolic properties of the heart. Diffuse foci of fibrosis in the myocardium have been reported with advancing age. Aldosterone has been shown to play a crucial role in the development of cardiac fibrosis via a direct effect on the mineralocorticoid receptors within the myocardium. Unlike the situation with treatment of systolic heart failure, few clinical trials are available to guide the management of patients with diastolic heart failure. In the absence of controlled clinical trials, patient management is based on control of the physiological factors (blood pressure, heart rate, blood volume and myocardial ischaemia) that are known to exert important effects on ventricular relaxation. Aldosterone antagonists inhibit the deposition of collagen matrix in the myocardium, thereby targeting the basic pathophysiological mechanism of diastolic dysfunction. Thus, they appear to represent a promising therapeutic approach for this condition. Currently, only small clinical trials supporting this therapy are available and large clinical trials evaluating long-term outcomes in diastolic dysfunction are therefore needed.

Aged↗
PubMed2003

Myocardial collagen turnover in hypertrophic cardiomyopathy.

BACKGROUND: Myocardial interstitial fibrosis is a characteristic of hypertrophic cardiomyopathy (HCM). This study evaluates the collagen turnover in HCM and its impact on left ventricular (LV) diastolic function. METHODS AND RESULTS: Thirty-six HCM patients and 14 sex- and age-matched controls were studied. Collagen turnover was assessed as follows. By radioimmunoassay, a byproduct of collagen III synthesis (PIIINP) and 3 peptides resulting from collagen I synthesis (PICP and PINP) and degradation (ICTP) were measured. By ELISA, matrix metalloproteinases (MMPs) were determined, as follows: active MMP-2; active MMP-9; and MMP-1 as active, free (as active MMP-1 plus its precursor), and total (as free MMP-1 plus MMP-1/tissue inhibitor complexes). Tissue inhibitor of metalloproteinases-1 (TIMP-1) was also assayed. All patients underwent echocardiography. The difference in duration between transmitral forward (A) and pulmonary venous retrograde (AR) waves (A-Ar) was considered an estimate of passive diastolic function. Furthermore, restrictive or pseudonormal LV filling patterns were considered to identify patients with passive diastolic dysfunction. Patients had higher levels of PIIINP, ICTP, MMP-2, MMP-9, and total TIMP-1 than did controls. PIIINP was inversely related to LV end-diastolic diameter. A-Ar was inversely related to PICP, PINP, and their differences with ICTP (estimates of collagen I buildup). Furthermore, A-Ar was directly related to MMP-1 and MMP-2. CONCLUSIONS: As compared with controls, collagen turnover is enhanced in HCM patients. As collagen I synthesis prevails over degradation and MMP-1 and MMP-2 are inhibited, passive diastolic dysfunction occurs in patients with HCM.

Adult↗
PubMed2000

Essentials of the diagnosis of heart failure.

Although heart failure is a common clinical syndrome, especially in the elderly, its diagnosis is often missed. A detailed clinical history is crucial and should address not only current signs and symptoms of heart failure but also signs and symptoms that point to a specific cause of the syndrome, such as coronary artery disease, hypertension or valvular heart disease. It is important to determine whether the patient has had a previous cardiac event, in particular a myocardial infarction. The physical examination should include Valsalva's maneuver, a test that is highly specific and sensitive for the detection of left ventricular systolic and diastolic dysfunction in patients with heart failure. An electrocardiograph and a chest radiograph should also be obtained. Two-dimensional echocardiography of the heart helps differentiate systolic from diastolic dysfunction. Coronary angiography is indicated in patients with heart failure and anginal chest pain and should be strongly considered in patients with an electrocardiogram suggestive of ischemia or myocardial infarction.

Algorithms↗
PubMed2006

Selective aldosterone blockade suppresses atrial tachyarrhythmias in heart failure.

INTRODUCTION: Renin-angiotensin-aldosterone system activation may be involved in the pathogenesis of atrial arrhythmias in congestive heart failure (CHF). The effects of aldosterone blockade on atrial tachyarrhythmias have not been evaluated. This study's aim was to determine whether selective aldosterone blockade suppresses atrial tachyarrhythmia inducibility and modifies atrial electrical and/or structural remodeling in a canine model of rapid ventricular pacing (RVP)-induced CHF. METHODS AND RESULTS: Dogs were assigned randomly to treatment with oral placebo or eplerenone (50 mg/day) and divided into four groups: two sham-operated (no RVP) and two RVP groups. After 5 weeks of no RVP or RVP at 230 beats/min along with concurrent placebo or eplerenone treatment, dogs underwent electrophysiologic and echocardiographic studies. Sustained atrial tachyarrhythmia inducibility (>10-minute duration), atrial effective refractory periods (ERPs), systolic and diastolic function, and left atrial and left ventricular (LV) chamber sizes were assessed. Placebo-treated RVP dogs developed CHF with LV systolic and diastolic dysfunction, left atrial and LV enlargement, increased atrial ERPs, and inducible sustained atrial tachyarrhythmias. Eplerenone treatment in RVP dogs significantly suppressed sustained atrial tachyarrhythmia inducibility, nonuniformly prolonged atrial ERPs and attenuated LV diastolic dysfunction without modifying left atrial or LV dilation or ejection fractions in CHF. Isoproterenol (2-4 microg/min) reversed eplerenone's atrial antiarrhythmic and ERP prolonging effects in CHF. Eplerenone did not alter atrial ERPs in sham (no RVP) dogs without CHF. CONCLUSIONS: Eplerenone suppresses inducibility of sustained atrial tachyarrhythmias, selectively prolongs atrial ERPs, and attenuates LV diastolic remodeling in RVP-induced CHF. Aldosterone blockade may be a promising new approach for atrial tachyarrhythmia prevention in CHF.

Administration, Oral↗
PubMed2005

Transesophageal echocardiographic evaluation of diastolic function.

Diastolic dysfunction is increasingly recognized as a cause of hemodynamic instability in the perioperative setting. Difficulty weaning from cardiopulmonary bypass and an increased need for inotropic support can occur in the absence of systolic impairment. Diastolic dysfunction can also impede hemodynamic stabilization and weaning progress in the mechanically ventilated critically ill patient. The use of transesophageal echocardiography in the ICU can assist in diagnosing the presence and progression of diastolic impairment, which may help to target therapeutic interventions that lead to positive outcomes. This review summarizes the conventional and new echocardiographic modalities for evaluating diastolic function in the perioperative setting.

Algorithms↗
PubMed2006

Nesiritide for treatment of perioperative low cardiac output syndromes in cardiac surgical patients: an initial experience.

The physiologic properties of the b-type natriuretic peptide nesiritide include pulmonary, coronary, and renal arterial vasodilation and lusitropic effects on ventricular myocardium. These effects may be useful during cardiac surgery, particularly when myocardial function and cardiac output (CO) are compromised. Intraoperative hemodynamic data were collected retrospectively before and 5-15 min following completion of a nesiritide loading dose in 15 adult cardiac surgical patients with low CO associated with pulmonary hypertension, low left ventricular ejection fraction, diastolic dysfunction, or left ventricular assist device placement. In seven patients, prior alternative pharmacologic interventions had failed to improve CO, and fluid challenges were ineffective in six patients with diastolic dysfunction. Perioperative nesiritide administration (2 microg.kg(-1) load, followed by 0.01 microg.kg(-1).min(-1) for a maximum of 24 h) resulted in a statistically significant median increase in CO of 35% (P = 0.0006). In conclusion, nesiritide was associated with increased CO in patients with low CO syndromes undergoing cardiac surgery, when other measures failed. This novel agent may offer an additional option to inotropes and fluid challenges for these patients perioperatively. Randomized clinical trials are desirable to determine the risks and benefits of nesiritides and to elucidate its role for the cardiac anesthesiologist.

Aged↗
PubMed1997

Diastolic properties in canine hypertensive left ventricular hypertrophy: effects of angiotensin converting enzyme inhibition and angiotensin II type-1 receptor blockade.

OBJECTIVE: Angiotensin II has been suggested to be involved in the pathogenesis of diastolic dysfunction in left ventricular hypertrophy (LVH). The purpose of this study was to asses the effects of enalaprilat and L-158,809, an angiotensin II type-1 receptor antagonist, on LV diastolic function in 16 normal control dogs and 20 LVH dogs with perinephritic hypertension. METHODS: LV hemodynamics was studied before and after intravenous injection of enalaprilat (0.25 mg/kg) or L-158,809 (0.3 mg/kg). The hemodynamic data were analyzed in relation to the changes in myocardial blood flow (measured by radioactive microspheres) and in the circulating angiotensin II and norepinephrine levels. RESULTS AND CONCLUSIONS: At baseline, significant increases were observed for LV/body weight ratio as well as LV systolic and end-diastolic pressure in the LVH dogs (all P < 0.01 vs. the control group). In addition, LV relaxation time constant was prolonged and the chamber and myocardial stiffness constants were increased (P < 0.01) in the LVH dogs, suggesting an impairment of LV diastolic function. Administration of enalaprilat or L-158,809 improved LV stiffness constants in the LVH dogs (P < 0.05). The diastolic LV pressure-diameter relation shifted downwards in the LVH dogs whereas diastolic distensibility was not altered in the control dogs. Although the circulating angiotensin II levels were significantly decreased by enalaprilat in the LVH dogs, they did not correlate with the changes in the stiffness constants. Furthermore, the alterations of LV diastolic properties in the LVH group could not be attributed to myocardial perfusion, which was rather decreased by administration of enalaprilat and L-158,809. These results suggest that angiotensin II, particularly at the local level, is involved in the pathogenesis of diastolic dysfunction in pressure-overload LVH. The data also support the concept that ACE inhibitors and angiotensin II receptor blockers are potentially beneficial in the treatment of the hypertrophied heart.

Angiotensin II↗
PubMed1992

[Effects of captopril on left ventricular morphology and function in essential arterial hypertension].

BACKGROUND: The presence of diastolic dysfunction in a hypertensive patient is not necessarily associated to the existence of left ventricular hypertrophy. The aim of this study was to determine whether the reduction of the left ventricular mass in hypertensive patients treated with captopril is accompanied by an improvement of the diastolic filling indexes. METHODS: Nineteen patients with essential hypertension were studied before and after one year of treatment with captopril. Different morphological indexes and diastolic function of the left ventricle were evaluated by mode M and Doppler echography. RESULTS: The indexes of left ventricular mass diminished significantly with treatment with captopril. The thickness of the ventricular walls diminished with treatment although not significantly. No significant modification was observed in the indexes of diastolic function (quotient of speed of protodiastolic filling/speed of telediastolic filling and time of deceleration of transmitral fluid during diastole) following the treatment period. CONCLUSIONS: Diminution of the left ventricular mass induced by captopril in hypertensive patients is not accompanied by an improvement in ventricular filling. It is suggested that myocardial hypertrophy is not responsible for diastolic dysfunction of arterial hypertension.

Adult↗
PubMed2003

Expression of bradykinin receptors in the left ventricles of rats with pressure overload hypertrophy and heart failure.

OBJECTIVES: Bradykinin exerts cardioprotective effects through bradykinin type-2 receptors (BK-2Rs). After acute myocardial infarction in rat, the heart adapts by increasing its number of BK-2Rs. However, in human chronic end-stage heart failure, the number of BK-2Rs is significantly decreased. Thus, the presence of a cardioprotective BK-2R signaling system may be critical in the prevention of pressure overload-induced heart failure. DESIGN: To explain differences in myocardial BK-2R expression during cardiac overload, we studied: (1). spontaneously hypertensive rats (SHRs) of different ages, and (2). normotensive Sprague-Dawley rats subjected to aortic banding or angiotensin II infusion. METHODS AND RESULTS: The mRNA levels of BK-2Rs were found to be significantly (P < 0.05) increased in the aging (12 and 20-month-old) SHRs (2.9- and 3-fold, respectively). Similarly, in the Sprague-Dawley rats, the expression of BK-2Rs was increased at 12 h (1.8-fold, P < 0.05) and at 3 days (3.1-fold, P < 0.05) after aortic banding, and at 2 weeks (2.2-fold) after angiotensin II infusion. In the 12-month-old SHRs, with compensated left ventricular hypertrophy (no fibrosis or left ventricular dysfunction), the amount of BK-2Rs was also significantly increased (1.8-fold, P < 0.05). However, in the 20-month-old SHRs, with a dramatic increase in fibrosis and development of diastolic dysfunction and heart failure, the amount of BK-2Rs were significantly decreased (63%, P < 0.05) specifically in the cardiac endothelial cells. CONCLUSIONS: The present results show that, during pressure overload and compensated left ventricular hypertrophy, the expression of BK-2Rs is increased. However, ongoing pressure overload leads to a loss of BK-2Rs with a dramatic increase in left ventricular fibrosis followed by diastolic dysfunction and heart failure.

Angiotensin II↗
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↗