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PubMed2000

Pulmonary edema after cardioversion for paroxysmal atrial flutter: left ventricular diastolic dysfunction induced by direct current shock.

This report describes a patient with the pulmonary edema after cardioversion for paroxysmal atrial flutter without organic heart disease. A 68-year-old man was admitted to hospital for paroxysmal atrial flutter. Antiarrhythmic agents were not effective, and direct current cardioversion was performed on the 4th hospital day. Three hours after cardioversion, the patient complained of dyspnea, and a chest X-ray showed pulmonary edema. He responded to oxygen, intravenous furosemide and drip infusion of nitroglycerine. During tapering of the medication, his condition remained stable. The patient was discharged on the 7th day after admission. Echocardiographic findings indicated that transient left ventricular diastolic dysfunction due to direct current shock was the most likely cause of the lung edema.

Aged↗
PubMed1994

Left ventricular diastolic dysfunction in lymphocytic myocarditis as assessed by Doppler echocardiography.

Pulsed-wave Doppler echocardiography of left ventricular (LV) inflows was performed in 30 consecutive patients with biopsy-proven lymphocytic myocarditis. There were 21 men and 9 women (mean age 50 +/- 15 years). LV ejection fraction was < or = 30% in 73% of the patients. Sixty-six percent were in New York Heart Association functional class III to IV. Peak early (E) velocity, late (A) velocity, deceleration time and filling pattern were assessed. These values were compared with a control population. E velocity in lymphocytic myocarditis was significantly higher than in control subjects (79 +/- 34 vs 67 +/- 14 cm/s, p = 0.0034). A velocity was lower in patients with myocarditis than in control subjects (38 +/- 20 vs 49 +/- 12 cm/s, p = 0.0001). Correspondingly, the E/A ratio was greater in the myocarditis group (2.5 +/- 1.3 vs 1.5 +/- 0.5, p < 0.0001). In particular, mean deceleration time in patients with myocarditis was significantly lower than that of control subjects (151 +/- 52 vs 194 +/- 30 ms, p < 0.0001). Diastolic filling patterns were abnormal in 29 of 30 patients (97%) with lymphocytic myocarditis, revealing a restrictive pattern in 25, abnormal relaxation in 4 and a normal pattern in 1. Lymphocytic myo-carditis is therefore associated with LV diastolic dysfunction of a predominantly restrictive pattern.

Adult↗
PubMedDate not supplied

Cardiac diastolic dysfunction in renal-transplant recipients is associated with increased circulating Adrenomedullin.

BACKGROUND: Renal transplantation is an excellent therapeutic alternative for end-stage renal diseases. Nevertheless, the cardiac function is often impaired in renal-transplant patients (RTR) and importantly determines their prognosis. Adrenomedullin (ADM), a peptide involved in cardiovascular homeostasis, is believed to protect both cardiac and renal functions - by increasing local blood flows, attenuating the progression of vascular damage and remodelling and by reducing glomerular injury - and might be involved in renal-transplantation physiopathology. This work was performed to investigate whether an increase in circulating ADM might be related to RTR cardiac function. METHODS: Twenty-nine subjects, 19 RTR and 10 healthy subjects, participated in the study. After 15 min rest in supine position, heart rate and systemic blood pressure were measured together with cyclosporine through levels, creatinine and ADM. Systolic and diastolic cardiac functions were assessed, using Doppler echocardiography. RESULTS: Subjects were similar concerning age, weight, heart rate and blood pressure. Creatinine and ADM (53.8 +/- 6.9 vs. 27.2 +/- 4.1 pmol/L, p = 0.02) were significantly increased in RTR (73 +/- 10 months after transplantation). Cardiac systolic function was normal, but a reduced mitral E:A ratio was observed in RTR (0.90 +/- 0.06 vs. 1.38 +/- 0.10, p < 0.001), reflecting their impaired left ventricular relaxation. Such a ratio was negatively correlated with ADM (r = -0.55, p = 0.002). CONCLUSIONS: RTR present with an increased ADM is likely related to cardiac diastolic dysfunction. In view of its protective effect on the cardiovascular system, these data support further studies to better define the role and the therapeutic potential of ADM after renal transplantation.

Adrenomedullin↗
PubMedDate not supplied

Diastolic dysfunction and mortality in diabetic patients on hemodialysis: a 4.25-year controlled prospective study.

Among patients on hemodialysis, the mortality rate is higher in individuals with diabetes than in nondiabetic individuals, especially due to cardiovascular causes. The objective of the present study was to evaluate the role of echocardiographic abnormalities to predict mortality in diabetic patients starting hemodialysis. A 4.25-year prospective study was carried out with 40 diabetic and 28 nondiabetic patients starting hemodialysis in five dialysis centers in the metropolitan area of Porto Alegre, Brazil, between August 1996 and June 1999. Cardiovascular status was evaluated based on World Health Organization criteria, resting electrocardiogram (ECG), myocardial scintigraphy (at rest and after dipyridamole administration), and M-mode and Doppler echocardiography. Left ventricular diastolic function was classified into the following filling patterns: normal, impaired relaxation, pseudonormal, or restrictive. The survival rate was analyzed by Kaplan-Meier curves and predictors of death by Cox's proportional-hazards model. At the end of the study, the overall mortality rate was higher in patients with diabetes [19/40 (47.5%)] than in those without diabetes [2/28 (7.1%), P=.0013, log rank test]. Pseudonormal and restrictive filling patterns (HR: 3.2; 95% CI: 1.2-8.8; P=.02) and presence of diabetes (HR: 4.7; 95% CI: 1.03-21.4; P=.04) were associated with mortality. In conclusion, left ventricular diastolic dysfunction (LVDD) was the main predictor of mortality in this cohort of diabetic and nondiabetic patients starting dialysis. Intensive treatment of cardiovascular risk factors before the start of dialysis and during the treatment might reduce the mortality rate in diabetic patients.

Adult↗
PubMed1990

Abnormal intracellular calcium handling in acute and chronic heart failure: role in systolic and diastolic dysfunction.

Acute or chronic heart failure may be caused by one or more of a variety of abnormalities including changes in excitation-contraction coupling processes (i.e. decreased availability of activator Ca2+ or a change in myofilament Ca2+ responsiveness), a change in myocardial energetics, or a change in extracellular factors, such as connective tissue content. Most of the animal and human models of acute cardiac failure that we have studied in our laboratory (i.e. negative inotropic responses to drugs, hypoxia, acidosis and ischaemia) appear to involve changes in excitation-contraction coupling as the predominant cause of dysfunction. On the other hand, the models of chronic cardiac dysfunction that we have studied (i.e. chronic right ventricular pressure overload in ferrets, hypertrophic cardiomyopathy in Syrian hamsters, hypertensive cardiomyopathy in rats, hypothyroidism in ferrets, end-stage dilated and hypertrophic cardiomyopathy in man) predominantly appear to reflect a combination of changes involving abnormalities in both excitation-contraction coupling and extracellular factors involving myocyte drop-out and increases in connective tissue content. However. In most of these models of acute and chronic heart failure, abnormal intracellular Ca2+ handling appears to be a major cause of both systolic and diastolic dysfunction.

Acute Disease↗
PubMedDate not supplied

Diastolic dysfunction in arterial hypertension.

Left ventricular diastolic properties are important markers of pump function and are frequently abnormal when myocardial insults alter tissue structure. Alterations can be limited to the early diastolic phase (early active relaxation) or to late diastolic filling (late ventricular compliance), but more often involve regulation of both phases of diastole. In asymptomatic patients with arterial hypertension, left ventricular relaxation is often prolonged, independently, at least in part, of cardiac loading conditions and left ventricular geometry, but this abnormality is associated with early signs of systolic dysfunction. Uncontrolled hypertension, diabetes, and obesity are most often associated with ischemic heart disease and impaired diastolic function. Reducing blood pressure with antihypertension therapy will reduce myocardial afterload, regress LVH, and improve systolic and diastolic function. In patients with symptoms of CHF with a normal ejection fraction, however, changes in therapy may be indicated. Greater emphasis should be placed on using medications that decrease myocardial load, but also reduce the effects of neurohormonal activation. (c)2001 by Le Jacq Communications, Inc.

Antihypertensive Agents↗
PubMed1993

Congestive heart failure from left ventricular diastolic dysfunction in systemic hypertension.

Previous studies have pointed out that congestive heart failure (CHF) with normal ejection fraction presents a uniform clinical profile that is indistinguishable from heart failure with low ejection fraction. Thirty-six patients with systemic hypertension who had recently experienced CHF with normal ejection fraction (> or = 50%) and no clinical history of ischemic cardiomyopathy were studied. The patients were divided into 2 groups according to degree of echocardiographic hypertrophy: group A (19 patients) with a ventricular mass/volume ratio > 1.8, and group B (17 patients) with a ratio < 1.8. Group A patients had a higher ejection fraction (67 +/- 6 vs 57 +/- 3%, p < 0.01), smaller ventricular diameters and a lower thallium-201 positive rate at peak stress (10 vs 70% in group B, p < 0.001), with 8 of 10 showing severe coronary stenosis. Clinically, group A had a more frequent audible fourth sound (79 vs 17%, p < 0.001), a low incidence of audible third sound (5 vs 55%, p < 0.001) and a cardiothoracic ratio < or = 0.5 (63 vs 17%, p < 0.01). The degree of radionuclide-detected resting diastolic dysfunction and exercise intolerance was similar in both groups. In conclusion, CHF with normal ejection fraction in hypertensive patients presents 2 different profiles: one characterized by severe hypertrophy and the other by a high rate of myocardial regional ischemia. Therapy should be aimed at pathophysiologic regression of the hypertrophy in the first case, and at improvement of the ischemia in the second.

Aged↗
PubMed1997

Contractile systolic and diastolic dysfunction in renin-induced hypertensive cardiomyopathy.

The present study investigated whether functional, molecular, and biochemical alterations occurring in chronic heart failure can already be detected in compensated hypertensive cardiac hypertrophy. Force of contraction (isolated papillary muscle strip preparations), sarcoplasmic reticulum (SR) protein and myosin heavy chain isoform expression (Northern and Western blot analysis), myocardial fibrosis (collagen stains, hydroxyproline quantification), myocardial renin mRNA (RT-PCR), and angiotensin II levels and plasma aldosterone concentrations (radioimmunoassay) were studied in hypertrophied myocardium from transgenic rats harboring the mouse Ren-2d gene. Contraction and relaxation velocities of isolated papillary muscle strips were significantly reduced in cardiac hypertrophy. The beta-/alpha-myosin heavy chain ratio was significantly increased in the hypertrophied left ventricles, whereas SR Ca2+-ATPase (SERCA 2a) and phospholamban mRNA and protein levels were significantly decreased. The decrease in SERCA 2a was more pronounced than the decrease in phospholamban levels. There was no increased myocardial fibrosis. Left ventricular myocardial renin mRNA and angiotensin II concentrations, as well as plasma aldosterone levels, were higher in transgenic than in control rats. In hypertensive cardiac hypertrophy, myosin heavy chain isoform shift and reduction of SR protein levels are related to systolic and diastolic dysfunction, respectively. These alterations precede the development of myocardial fibrosis. Increased myocardial renin mRNA and angiotensin II concentrations suggest that an activated tissue renin-angiotensin system might contribute to these alterations. Since the alterations in compensated cardiac hypertrophy apparently precede those in chronic heart failure, they might accelerate the transition from hypertrophy to failure and could therefore be targets for pharmacological interventions.

Angiotensin II↗
PubMed2005

Mineralocorticoid receptor antagonism ameliorates left ventricular diastolic dysfunction and myocardial fibrosis in mildly symptomatic patients with idiopathic dilated cardiomyopathy: a pilot study.

BACKGROUND: Mineralocorticoid receptor antagonism reduces mortality associated with heart failure by mechanisms that remain unclear. The effects of the mineralocorticoid receptor antagonist spironolactone on left ventricular (LV) function and chamber stiffness associated with myocardial fibrosis were investigated in mildly symptomatic patients with idiopathic dilated cardiomyopathy (DCM). METHODS AND RESULTS: Twenty-five DCM patients with a New York Heart Association functional class of I or II were examined before and after treatment with spironolactone for 12 months. LV pressures and volumes were measured simultaneously, and LV endomyocardial biopsy specimens were obtained. Serum concentrations of the carboxyl-terminal propeptide (PIP) and carboxyl-terminal telopeptide (CITP) of collagen type I were measured. The patients were divided into 2 groups on the basis of the serum PIP/CITP ratio (< or =35, group A, n=12; >35, group B, n=13), an index of myocardial collagen accumulation. LV diastolic chamber stiffness, the collagen volume fraction, and abundance of collagen type I and III mRNAs in biopsy tissue were greater and the LV early diastolic strain rate (tissue Doppler echocardiography) was smaller in group B than in group A at baseline. These differences and the difference in PIP/CITP were greatly reduced after treatment of patients in group B with spironolactone, with treatment having no effect on these parameters in group A. The collagen volume fraction was significantly correlated with PIP/CITP, LV early diastolic strain rate, and LV diastolic chamber stiffness for all patients before and after treatment with spironolactone. CONCLUSIONS: Spironolactone ameliorated LV diastolic dysfunction and reduced chamber stiffness in association with regression of myocardial fibrosis in mildly symptomatic patients with DCM. These effects appeared limited, however, to patients with increased myocardial collagen accumulation.

Adult↗
PubMed1994

Systolic and diastolic dysfunction in patients with clinical diagnosis of dilated cardiomyopathy. Relation to symptoms and prognosis.

BACKGROUND: Dilated cardiomyopathy is an important cause of morbidity and mortality among patients with congestive heart failure. Hemodynamic and prognostic characterization are critical in guiding selection of medical and surgical therapies. METHODS AND RESULTS: A cohort of 102 patients with the clinical diagnosis of dilated cardiomyopathy who underwent echocardiographic examination between 1986 and 1990 was identified and followed up through July 1, 1991. Patients with moderate or severe symptoms had lower indices of systolic function and greater left atrial and right ventricular dilation. Mitral inflow Doppler signals were characterized by a restrictive left ventricular filling pattern. In multivariate logistic regression analysis, deceleration time, ejection fraction, and peak E velocity were independently associated with symptom status. Over a mean follow-up of 36 months, 35 patients died. Kaplan-Meier estimated survival at 1, 2, and 4 years was 84%, 73%, and 61%, respectively, and was significantly poorer than that of an age- and sex-matched population. The subgroup with an ejection fraction < 0.25 and deceleration time < 130 milliseconds had a 2-year survival of only 35%. The subgroup with ejection fraction < 0.25 and deceleration time > 130 milliseconds had an intermediate 2-year survival of 72%, whereas patients with an ejection fraction > or = 0.25 had 2-year survivals > or = 95% regardless of deceleration time. In multivariate analysis, ejection fraction and systolic blood pressure were independently predictive of subsequent mortality. Mitral deceleration time was significant in univariate analysis. CONCLUSIONS: In patients with the clinical diagnosis of dilated cardiomyopathy, markers of diastolic dysfunction correlated strongly with congestive symptoms, whereas variables of systolic function were the strongest predictors of survival. Consideration of both ejection fraction and deceleration time allowed identification of subgroups with divergent long-term prognoses.

Aged↗
PubMed2005

Myocardial stiffness, cardiac remodeling, and diastolic dysfunction in calcification-prone fetuin-A-deficient mice.

Accelerated atherosclerosis in dialysis patients is characterized by severe vascular calcification, and the magnitude of vascular calcification is associated with increased cardiovascular mortality. Calcification-dependent arterial stiffness is considered to be a major determinant of cardiac failure in uremia. Fetuin-A/alpha(2)-Heremans-Schmid glycoprotein is an abundant serum protein with powerful calcification inhibitory properties. Fetuin-A deficiency was recently linked to cardiovascular mortality in dialysis patients. Fetuin-A knockout (fetuin-KO) mice spontaneously develop widespread soft tissue calcification, including significant myocardial calcification, whereas larger arteries are spared. Therefore, this investigation offers the unique opportunity to study the functional role of isolated myocardial calcification independent of arterial stiffness by assessing the hemodynamics of fetuin-KO mice. Cardiac output in fetuin-KO mice was lower than in wild-type mice (fetuin-KO 1.81 +/- 0.18 versus WT 2.45 +/- 0.29 ml/min per g; P < 0.005), and fetuin-KO mice were refractory to dobutamine stimulation. Left ventricular relaxation was significantly impaired in fetuin-KO hearts with the relaxation index reduced by 23% (P < 0.005). After ischemia, fetuin-KO hearts displayed a continuous decline in left ventricular developed pressure after the initial phase of reperfusion, resulting in 77 +/- 15% of preischemic left ventricular developed pressure (P < 0.05 versus wild-type). In fetuin-KO mice, dystrophic cardiac calcification, with myocardial calcium contents increased 60-fold, was associated with profound induction of profibrotic TGF-beta and downstream collagen and fibronectin mRNA synthesis. In conclusion, independent of arterial stiffness, calcification-associated "myocardial stiffness" characterized by cardiac fibrosis, diastolic dysfunction, impaired tolerance to ischemia, and catecholamine resistance thus may constitute an underestimated cardiovascular risk factor that contributes to cardiac failure in calcification-prone states.

Animals↗
PubMed2000

Pretreatment with growth hormone-releasing peptide-2 directly protects against the diastolic dysfunction of myocardial stunning in an isolated, blood-perfused rabbit heart model.

Brief coronary occlusion followed by reperfusion leads to reversible myocardial dysfunction (stunning) which can induce irreversible damage of other organ systems. We studied the effects of pretreatment with recombinant human GH (rhGH) and the GH-secretagogue GHRP-2 on myocardial stunning in a blood-perfused isolated rabbit heart model. In a first set of experiments, effects of bolus rhGH administration (3.5 mg/kg) (n = 5) into the aortic root of unpretreated animals were compared with those of saline (n = 6). In a second set, animals were pretreated for 14 days with SC rhGH 3.5 mg/kg x day (n = 9) or 160 microg/kg x day GHRP-2 (n = 8) in two divided doses. Body weight and plasma concentrations of rhGH, rabbit GH (rGH) and IGF-I were determined before and at the end of 14 days pretreatment. Hearts were excised and submitted to 15 min ischemia followed by 80 min reperfusion, after which postischemic recovery was compared with nonischemic hearts mounted into the same system. At study end, all hearts were snap-frozen to examine markers of apoptosis. Circulating levels of rabbit GH (rGH) remained identical in all animals. Pretreatment with rhGH for 14 days induced a 142 +/- 116% rise of serum IGF-I vs. 8 +/- 15% with GHRP-2 (P < 0.001) and increased body weight with 6.8 +/- 2.5% vs. 3.4 +/- 3.3% with GHRP-2 (P = 0.01). A bolus injection of rhGH did not alter myocardial function compared with saline allowing data from these experiments to be pooled into one ischemic control group for further analysis of the effect of pretreatment. No difference in postischemic recovery of left ventricular systolic function among the unpretreated, rhGH pretreated and GHRP-2 pretreated hearts was apparent. At the end of reperfusion, a 3-fold higher end-diastolic pressure (EDP) persisted in the unpretreated and rhGH pretreated hearts compared with the nonischemic hearts. In the GHRP-2 pretreated hearts, EDP decreased to half the pressure observed in unpretreated and rhGH pretreated hearts (all P < or = 0.02), a level which was indistinguishable from that in the non-ischemic hearts, suggesting full postischemic recovery of diastolic function. There were no signs of increased apoptosis in the experimental groups. In conclusion, 14 days pretreatment with GHRP-2, but not rhGH, protected selectively against the diastolic dysfunction of myocardial stunning in this model. This observation may open perspectives for GH-secretagogues as cardioprotective agents.

Animals↗
PubMed1992

[Precocity of diastolic dysfunction in hypertensive cardiopathy].

Left ventricular hypertrophy (LVH) is a well defined cardiovascular risk factor and is frequently detected by echocardiography in hypertensive patients. Systolic cardiac function at rest is usually preserved in hypertension, however, diastolic function may be frequently altered. Evidence for these changes has been demonstrated by Echo-Doppler even without concomitant existence of LVH. Quantitative and qualitative changes in contractile proteins and interstitial tissue as well as reduction of coronary reserve may be related to the mentioned dysfunction. Recent studies have confirmed the precocity of diastolic dysfunction both in laboratory animals as well as man. Further significant differences have been shown between normotensives with and without a family history of systemic hypertension. The relative importance of diastolic disfunction is also related to its possible role in the genesis of cardiac failure and its probable role in the modulation of cardiopulmonary reflexes in addition to the hemodynamics of arterial hypertension. It is not yet known if the presence of diastolic dysfunction is a mechanism or a risk marker like LVH.

Cardiomegaly↗
PubMed2007

Differential impact of atorvastatin vs pravastatin on progressive insulin resistance and left ventricular diastolic dysfunction in a rat model of type II diabetes.

BACKGROUND: Controversy exists regarding the effects of statin therapy on progressive insulin resistance (IR) and its consequences, in the present study a rat model of spontaneously developing type II diabetes mellitus (DM) was used to examine the impact of atorvastatin (AS) vs pravastatin (PS). METHODS AND RESULTS: The Otsuka Long-Evans Tokushima Fatty rats were either untreated or treated with 100 mg/kg per day of AS or PS from 6 weeks of age for 24 weeks. AS achieved much greater lipid lowering than PS. Serial oral glucose tolerance tests revealed new-onset diabetes was delayed by PS only. The untreated rats exhibited a progressive decrease in plasma adiponectin, increases in plasma leptin and tumor necrosis factor-alpha, and reduction of plasma nitric oxide (NO), which were limited more by PS than AS. PS, but not AS, enhanced adiponectin mRNA expression in white adipose tissue at 30 weeks. Cardiac endothelial NO synthase expression was upregulated, and overexpression of both transforming growth factor-beta1 and monocyte chemoattractant protein-1 mRNA was limited more by PS than AS. Coronary perivascular fibrosis at 30 weeks was suppressed only by PS, which was accompanied by preserved left ventricular diastolic function assessed with Doppler echocardiography. CONCLUSIONS: The moderate lipid lowering by PS, but not the intensive lipid lowering by AS, prevented new-onset DM and diastolic dysfunction in a rat model of IR, and this was associated with preferable adipocytokine profiles and cardiac redox states.

Adiponectin↗
PubMed2005

Aging induces cardiac diastolic dysfunction, oxidative stress, accumulation of advanced glycation endproducts and protein modification.

Evidence suggests that aging, per se, is a major risk factor for cardiac dysfunction. Oxidative modification of cardiac proteins by non-enzymatic glycation, i.e. advanced glycation endproducts (AGEs), has been implicated as a causal factor in the aging process. This study was designed to examine the role of aging on cardiomyocyte contractile function, cardiac protein oxidation and oxidative modification. Mechanical properties were evaluated in ventricular myocytes from young (2-month) and aged (24-26-month) mice using a MyoCam system. The mechanical indices evaluated were peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocity of shortening/relengthening (+/- dL/dt). Oxidative stress and protein damage were evaluated by glutathione and glutathione disulfide (GSH/GSSG) ratio and protein carbonyl content, respectively. Activation of NAD(P)H oxidase was determined by immunoblotting. Aged myocytes displayed a larger cell cross-sectional area, prolonged TR90, and normal PS, +/- dL/dt and TPS compared with young myocytes. Aged myocytes were less tolerant of high stimulus frequency (from 0.1 to 5 Hz) compared with young myocytes. Oxidative stress and protein oxidative damage were both elevated in the aging group associated with significantly enhanced p47phox but not gp91phox expression. In addition, level of cardiac AGEs was approximately 2.5-fold higher in aged hearts than young ones determined by AGEs-ELISA. A group of proteins with a molecular range between 50 and 75 kDa with pI of 4-7 was distinctively modified in aged heart using one- or two-dimension SDS gel electrophoresis analysis. These data demonstrate cardiac diastolic dysfunction and reduced stress tolerance in aged cardiac myocytes, which may be associated with enhanced cardiac oxidative damage, level of AGEs and protein modification by AGEs.

Aging↗
PubMed1996

Left-ventricular diastolic dysfunction during pneumonectomy--a transesophageal echocardiographic study.

Left-ventricular dysfunction, with acute increase in capillary pulmonary pressure, can unexpectedly develop in patients submitted to pneumonectomy. In order to study the morphofunctional modifications induced by pneumonectomy on the left cardiac chambers, we performed intraoperative transesophageal echocardiography (TEE) in 8 patients (7 males, mean age 66 years) undergoing pneumonectomy for lung cancer. No patient had any cardiac involvement before surgery. The opening of the pericardium was associated with a slight paradoxical movement of the basal interventricular septum. After ligature of the pulmonary artery, the interventricular septum changed its geometry, losing the normal curvature and becoming rectilinear. These changes were related to an increase in right-ventricular (RV) dimensions. In all patients the pulmonary vein flow-profile (pulsed Doppler) showed an increased turbulence, associated with a reduced amplitude (5 patients) or an inversion (3 patients) of the second systolic component and with the development of mild mitral regurgitation (color Doppler). These changes disappeared at the end of intervention, before chest closure. No alteration in left-ventricular systolic function was found. These results suggest that the altered geometry of the interventricular septum, mainly due to acute RV overload, induces a transient left-ventricular diastolic dysfunction, associated with mild mitral regurgitation.

Aged↗
PubMed2006

Diastolic dysfunction and diabetic cardiomyopathy: evaluation by Doppler echocardiography.

Doppler echocardiography has largely contributed to show the existence of a distinct diabetic cardiomyopathy. Several studies have pointed out the evidence of left ventricular (LV) remodeling and hypertrophy in alterations of both midwall systolic mechanics and LV diastolic filling in diabetes mellitus (DM), independent of the coexistence of concomitant risk factors. Further progress will be provided by new ultrasound technologies in this clinical setting. The combination of pulsed tissue Doppler study of mitral annulus with transmitral inflow may be clinically valuable for obtaining information about left ventricular filling pressure (LVFP) and unmasking Doppler inflow pseudonormal pattern, a hinge point for the progression toward advanced heart failure. In the absence of epicardial coronary artery stenosis, the ultrasound assessment of coronary flow reserve (CFR) may identify the dysfunction of coronary microcirculation, in relation with glycemic levels, insulin resistance, sympathetic overdrive, endothelial dysfunction, abnormalities of the angiotensin-renin system, and LV remodeling/hypertrophy. Diastolic dysfunction and impairment of CFR may be associated in DM, with a likely common origin. In this view, a comprehensive transthoracic Doppler evaluation of diabetic patients should include the assessment of diastolic function and estimation of LVFP by tissue Doppler, and coronary microvascular function by CFR test. Additional analysis of regional wall motion during a stress test would be required in patients with suspected coronary artery disease, another cause of diastolic dysfunction.

Coronary Circulation↗
PubMed2002

Nipradilol can prevent left ventricular systolic and diastolic dysfunction after myocardial infarction in rats.

The purpose of this study was to examine the effects of nipradilol on the cardiac function and mRNA expression in Wistar rats with a myocardial infarction (MI) that was created by ligation of the anterior descending coronary. Ten mg x kg(-1) x day(-1) of nipradilol were administrated to the rats in random order, and hemodynamic and Doppler-echocardiographic findings and myocardial mRNA expression were analyzed at 4 weeks after MI. Although left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) were increased in the MI rats, nipradilol significantly reduced the degree of the increase in both parameters. MI also significantly increased the weight of the left and right ventricles, and increased the left ventricular end-diastolic dimension (LVDd), effects that were attenuated by nipradilol. The MI rats showed decreased fractional shortening as systolic dysfunction and decreased E wave deceleration rate as diastolic dysfunction, and nipradilol significantly prevented these. Nipradilol significantly suppressed the increase in the non-infarcted myocardial mRNA expression of atrial natriuretic peptide, brain natriuretic peptide and collagen I and III. In conclusions, nipradilol prevents the cardiac remodeling that is accompanied by systolic and diastolic dysfunction, and inhibits abnormal myocardial gene expression after MI.

Adrenergic beta-Antagonists↗