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PubMed1989

Influence of hypertension with minimal hypertrophy on diastolic function during demand ischemia.

Hearts with advanced pressure-overload hypertrophy from systemic hypertension have been shown to have an increased susceptibility to the development of diastolic dysfunction in response to tissue hypoxia and ischemia. It is not known if this propensity to develop diastolic dysfunction in response to ischemia is dependent on the presence of a substantial increase in left ventricular mass, or alternatively, is characteristic of hearts subjected to mild chronic hypertension early in the development of cardiac hypertrophy. We tested the hypothesis that systemic hypertension associated with mild left ventricular hypertrophy increases the susceptibility to the development of diastolic dysfunction in response to demand ischemia. The effects of demand ischemia (6 minutes) were studied in hearts from New Zealand white rabbits with chronic systemic hypertension produced by the one-kidney, one-wrap method (n = 15) and compared with age-matched, sham-operated control rabbits (n = 11) with similar left ventricular mass (5.4 +/- 0.2 vs. 5.4 +/- 0.3 g, respectively). The hearts were studied using an isolated, isovolumic (balloon in left ventricle) preparation with absent pericardium that was perfused with fresh whole blood. At baseline, coronary perfusion pressure was 100 mm Hg with comparable coronary flow per gram left ventricular weight; the hearts were paced at a physiological rate of 3 Hz, and the left ventricular balloon volume was adjusted to achieve a left ventricular end-diastolic pressure of 15 mm Hg in both groups. Left ventricular balloon volume was similar in both groups and volume was thereafter held constant. At baseline, left ventricular systolic pressure (114 +/- 4 vs. 95 +/- 3 mm Hg, p less than 0.001) and developed pressure (18.9 +/- 1.2 vs. 15.1 +/- 0.9 mm Hg/g, p less than 0.05) were higher in the hearts from the hypertensive group in comparison with the control group. During the first minute of global ischemia produced by reducing coronary perfusion pressure from 100 to 20 mm Hg, there was an immediate fall in left ventricular systolic pressure in both groups without an increase in diastolic pressure. In response to the superimposition of pacing tachycardia (heart rate, 6 Hz) during the remaining 5 minutes of the period of ischemia, left ventricular developed pressure was comparable. However, isovolumic left ventricular end-diastolic pressure (measured during long diastoles obtained with transient cessation of pacing) rose to a significantly higher level in the hearts from hypertensive rabbits than in those from the control rabbits (29 +/- 3 vs. 18 +/- 2 mm Hg, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

[A pulsed Doppler study of left atrial and ventricular inflow in 2 populations of normotensive and hypertensive subjects].

OBJECTIVE: Comparative analysis of left atrial and left ventricle Doppler inflow patterns in patients with essential systemic mild to moderate hypertension and normal global left ventricular systolic function. PATIENTS: A group of out patients with the diagnosis of hypertension referred to the Echocardiographic Laboratory of Egas Moniz Hospital in Lisbon. SETTING: Echocardiographic Doppler prospective study. MATERIAL AND METHODS: We studied a group of 50 patients with the diagnosis of mild to moderate arterial hypertension (Group H), which was compared with a population of 50 normal subjects (Group N). In each case we analysed the pulsed Doppler flow of the right upper pulmonary vein and the diastolic inflow of the left ventricular cavity. We calculated the peak velocities and time velocity integrals of the systolic, diastolic and atrial contraction waves of the pulmonary venous flow and also the systo-diastolic velocity and time velocity integral ratios. In the transmitral Doppler flow analysis we evaluated the peak velocities and time velocity integrals of the early (E wave) and late (A wave) waves, and their time velocity and velocity ratio. We assessed also the isovolumic relaxation time and left ventricular mass index. RESULTS: In groups N and H the peak velocity of the pulmonary venous flow systolic wave was 0.53 +/- 0.15 cm/sec and 0.75 +/- 0.10 cm/sec (p = 0.01), diastolic wave was 0.50 +/- 0.10 cm/sec and 0.41 +/- 0.09 cm/sec (p = 0.03) and atrial contraction wave was 0.18 +/- 0.03 cm/sec and 0.35 +/- 0.08 (p = 0.001), with a systo-diastolic ratio of 1.06 +/- 0.10 and 1.83 +/- 0.10 (p < 0.001), respectively. In these two groups the time velocity integral of the pulmonary venous flow systolic wave was 14.4 +/- 2.6 cm and 17.8 +/- 1.8 cm (p = 0.001), the diastolic wave was 12.5 +/- 3.2 cm and 9.3 +/- 1.3 cm (p = 0.05) and the atrial contraction wave was 4.4 +/- 0.07 cm (p = 0.001), with a systo-diastolic ratio of 1.1 +/- 0.16 and 1.9 +/- 0.12 (p < 0.001), respectively. For the group H and considering the three subgroups, hypertensive patients without anatomical or functional alterations, with isolated diastolic dysfunction and with left ventricular hypertrophy associated to diastolic dysfunction, the velocity systo-diastolic ratio was 1.08 +/- 0.12, 1.57 +/- 0.08 (p < 0.01) and 2.4 +/- 0.08 (p < 0.01) and 2.4 +/- 0.08 (p < 0.001), the systo-diastolic time velocity integral ratio was 1.22 +/- 0.17, 1.72 +/- 0.13 (p < 0.01) and 2.4 +/- 0.15 (p < 0.001), the peak velocity of the atrial contraction wave was 0.28 +/- 0.07, 0.3 +/- 0.08 (p < 0.01) and 0.43 +/- 0.07 (p < 0.001) and its time velocity integral was 4.6 +/- 0.06 cm, 5.6 +/- 0.07 cm (p < 0.01) and 7.0 +/- 0.08 cm (p < 0.001). CONCLUSIONS: Pulsed Doppler study of pulmonary venous flow is significantly abnormal in patients with arterial hypertension. This abnormal pulmonary venous flow pattern has a close relationship with structural and functional alterations of the left ventricle. Combined analysis of the pulsed Doppler inflow at these two cardiac anatomical levels is fundamental to understand the pathophysiology of hypertensive heart disease.

Adult↗
PubMed2002

Fetal cardiomyopathies: pathogenic mechanisms, hemodynamic findings, and clinical outcome.

BACKGROUND: Although the prenatal diagnosis of most fetal structural heart defects and dysrhythmias has been described, there is a paucity of information about cardiomyopathies (CMs) in prenatal life. METHODS AND RESULTS: To determine the pathogenic mechanisms, hemodynamic findings, and outcome of fetal CM, we reviewed the fetal echocardiograms and perinatal histories of 55 affected fetuses. Dilated CM was diagnosed in 22 cases, including 2 with congenital infections, 5 familial cases, 6 with endocardial fibroelastosis related to maternal anti-Ro/La antibodies, and 9 idiopathic cases. Thirty-three had hypertrophic CM, 7 associated with maternal diabetes, 2 with Noonan's syndrome, 2 with alpha-thalassemia, 18 with twin-twin transfusion syndrome, 1 with familial hypertrophy, and 3 with idiopathic hypertrophy. Systolic dysfunction was present in all cases of dilated CM and 15 cases of hypertrophic CM. Diastolic dysfunction was present in 19 of 30 fetuses with assessment of diastolic function parameters. Significant mitral or tricuspid valve regurgitation was seen in 32 cases. Eight fetuses were hydropic and 23 had signs of early hydrops. Seven pregnancies were terminated. Of 46 continued pregnancies with follow-up, 29 (63%) died perinatally. The presence of systolic dysfunction, diastolic dysfunction, and significant atrioventricular valve regurgitation were identified as risk factors for mortality. By multiple logistic regression, diastolic dysfunction was associated with an 8-fold increased risk relative to the other parameters. CONCLUSIONS: Fetal CM has a broad spectrum of intrinsic and extrinsic causes. A poor outcome is observed in many affected fetuses. Diastolic dysfunction in fetal CM is associated with the highest risk of mortality.

Cardiomyopathies↗
PubMedDate not supplied

Simulation of systolic and diastolic left ventricular dysfunction in a mock circulation: the effect of arterial compliance.

Arterial compliance (AC) is expected to play a major role on cardiac efficacy by acute or long-term mechanisms. The aim of this study was to investigate the purely mechanical effect of AC on left ventricular (LV) performance, for different conditions of LV dysfunction (systolic versus diastolic). A hydraulic, Windkessel model of systemic circulation was used. LV function and aortic flow were simulated using a left ventricular assist device (LVAD). Two cases of LV dysfunction were simulated: Case A, systolic and Case B, diastolic dysfunction. In Case A, AC increased from 1.14 to 2.85 ml mm Hg(-1) leading to an increase in LVAD stroke volume up to 6%, while no significant effect was observed in Case B. LVAD systolic work was decreased by 4% in systolic and by 11% in diastolic LVAD dysfunction. The purely mechanical effect of AC changes on LVAD function was different between systolic and diastolic dysfunction. It might be expected that even an acute reduction in arterial stiffness could enhance LV performance by different means in systolic compared to diastolic dysfunction.

Arteries↗
PubMed2004

Assessment of diastolic function in patients with hypertrophic cardiomyopathy by Doppler tissue imaging.

OBJECTIVE: To determine the clinical application of pulsed Doppler tissue imaging in assessing the left ventricular diastolic function and in discriminating between normal subjects and patients with hypertrophic cardiomyopathy with various stages of diastolic dysfunction. METHODS: We measured the peak diastolic velocities of mitral annulus in 81 patients with hypertrophic cardiomyopathy with various stages of diastolic dysfunction and 50 normal volunteers by Doppler tissue imaging using the apical window at 2-chamber and long apical views, respectively. The myocardial velocities were determined with use of variance F statistical analysis. RESULTS: Early diastolic myocardial velocities of mitral annulus were higher in normal subjects than in patients with hypertrophic cardiomyopathy with either delayed relaxation, pseudonormal filling, or restrictive filling. However, peak myocardial velocities of mitral annulus during atrial contraction were similar in normal subjects and patients with hypertrophic cardiomyopathy. CONCLUSION: Doppler tissue imaging can directly reflect upon left diastolic ventricular function. Early phase of diastole was the best discriminator between control subjects and patients with hypertrophic cardiomyopathy.

Adult↗
PubMed1991

[Correlations between blood pressure, left ventricular hypertrophy, and left ventricular diastolic function in hypertensive patients].

We examined the relationship of hypertension to left ventricular hypertrophy (LVH) and left ventricular diastolic function by ambulatory blood pressure monitoring device and echocardiography. We studied 36 untreated hypertensive non-diabetic patients (16 males and 20 females) whose casual systolic blood pressure (CSBP) and/or diastolic blood pressure (CDBP) were higher than 140 mmHg and 90 mmHg, respectively. All patients were less than 65 years of age without organic heart disease. Resting systolic and diastolic blood pressures (RSBP, RDBP) were measured after lying in a supine position for 30 min by the auscultatory method. Ambulatory blood pressure was measured every 30 or 60 min for 24 hours by Colin ABPM 630, and the mean 24-hour ambulatory systolic and diastolic blood pressures (ASBP, ADBP) and the systolic and diastolic hyperbaric indices (SHI, DHI) were obtained. The left ventricular mass index (LVMI) was obtained as an indicator of LVH by M-mode echocardiography. The ratio of peak velocity of mitral inflow caused by atrial contraction to that of rapid inflow (A/R) was obtained as an indicator of the LV diastolic function by Doppler echocardiography. The coefficients of correlation between BP and the LVMI, and the A/R were determined. There were significant positive correlations between the LVMI and ASBP (r = 0.51, p < 0.005), the SHI (r = 0.49, p < 0.005), CSBP (r = 0.47, p < 0.01) and RSBP (r = 0.41, p < 0.05), however, there were no significant correlations between the LVMI and ADBP, the DHI, CDBP, RDBP and age. There were significant positive correlations between the A/R and ADBP (r = 0.44, p < 0.01), age (r = 0.40, p < 0.02), CSBP (r = 0.38, p < 0.05) and RDBP (r = 0.38, p < 0.05), however, no significant correlations between the A/R and ASBP, the SHI, DHI, RSBP and CDBP. Only a weak correlation was observed in all subjects between the LVMI and A/R, which was slightly improved by use of > 90 mmHg CSBP readings (r = 0.32). It was concluded that LVH is related mainly to continuous systolic hypertension, and that LV diastolic dysfunction is related mainly to continuous diastolic hypertension. Therefore, it was suggested that LVH and LV diastolic dysfunction in hypertensive patients are caused by different mechanisms.

Adult↗
PubMed1994

Endomyocardial gene expression during development of pacing tachycardia-induced heart failure in the dog.

Selective and specific changes in gene expression characterize the end-stage failing heart. However, the pattern and relation of these changes to evolving systolic and diastolic dysfunction during development of heart failure remains undefined. In the present study, we assessed steady-state levels of mRNAs encoding a group of cardiac proteins during the early development of left ventricular dysfunction in dogs with pacing-induced cardiomyopathy. Corresponding hemodynamic assessments were made in the conscious state in the same animals and at the same time points at baseline, after 1 week of ventricular pacing, and at the onset of clinical heart failure. Systolic dysfunction dominated after 1 week of pacing, whereas diastolic dysfunction was far more pronounced with the onset of heart failure. Atrial natriuretic factor mRNA was undetectable in 7 of 12 hearts at baseline but was expressed in all hearts at 1 week (P < .01 by chi 2 test), and it increased markedly with progression to failure (P = .05). Creatine kinase-B mRNA also rose markedly with heart failure (P < .01). Levels of mRNA encoding beta-myosin heavy chain, mitochondrial creatine kinase, phospholamban, and sarcoplasmic reticulum Ca(2+)-ATPase did not significantly change from baseline, despite development of heart failure. Additional analysis to determine if these mRNA changes were related to the severity of diastolic or systolic dysfunction revealed that phospholamban mRNA decreased in hearts with larger net increases in end-diastolic pressure (+19.2 +/- 1.9 mm Hg) compared with those hearts in which it did not change (+4.0 +/- 4.9, P < .02).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed2000

[Diastolic heart failure. Treatment].

THERAPEUTIC OPTIONS: Many therapeutic options are proposed for the treatment of diastolic heart failure although no consensus has been established. In experimental trials, several drugs have demonstrated a potentially beneficial effect on ventricular diastolic dysfunction and could be used for diastolic heart failure: nitrate derivatives, converting enzyme inhibitors, angiotensin II antagonists, spirolactones and bradycardia agents. CLINICAL PRACTICE: In everyday clinical practice, low-dose diuretics and treatments aimed at reducing the triggering factor leading to episodes of heart failure are used alone or in combination with treatments aimed at the underlying cause of the diastolic dysfunction: betablockers, calcium inhibitors or nitrate derivatives for ischemic heart disease, drug therapy for hypertension, anti-diabetes agents, anti-arrhythmic agents for atrial fibrillation. Digitalics are not indicated. In experimental trials, converting enzyme inhibitors and angiotensin II antagonists have demonstrated interesting properties for the left ventricle but to date are not warranted for diastolic heart failure. TREATMENT OF THE CAUSE: Due to the lack of consensus on the optimal treatment for diastolic heart failure, most clinicians rely on treating the underlying heart disease and triggering factors.

Adrenergic beta-Antagonists↗
PubMed1997

Plasma concentration of brain natriuretic peptide is related to diastolic function in hypertension.

1. The plasma brain natriuretic peptide (BNP) concentration is elevated in patients with essential hypertension and normal systolic function. This may be related to left ventricular hypertrophy or diastolic dysfunction, both of which commonly occur in hypertension. 2. Echocardiography was performed on 32 patients with newly diagnosed untreated mild-to-moderate hypertension (19 men, 13 women; mean +/- SD age 51 +/- 15 years; diastolic blood pressure 99 +/- 12 mmHg; systolic blood pressure 153.2 +/- 18.0 mmHg; plasma creatinine 86 +/- 15 mumol/L; creatinine clearance 92.2 +/- 20.5 mL/min; left ventricular mass index 116 +/- 28 g/m2; left ventricular ejection fraction 66 +/- 9%). A 15 mL peripheral venous blood sample was obtained at the time of echocardiography for radioimmunoassay of BNP. 3. Sixteen patients had abnormal Doppler transmittal flow (E/A ratio < 1) and a higher median plasma BNP concentration compared with those patients with E/A > or = 1 (12.9 vs 5.9 pmol/L, respectively; P = 0.006). The plasma BNP level correlated significantly with E/A ratio (r = -0.50; P = 0.035). Multivariate analysis showed that the E/A ratio is related to plasma BNP, independent of age and blood pressure. 4. Our results suggest that the plasma BNP level is influenced by diastolic dysfunction. Further studies are needed to determine whether assay of plasma BNP helps to identify patients with diastolic dysfunction.

Adult↗
PubMed2002

Functional analysis of a troponin I (R145G) mutation associated with familial hypertrophic cardiomyopathy.

Familial hypertrophic cardiomyopathy has been associated with several mutations in the gene encoding human cardiac troponin I (HCTnI). A missense mutation in the inhibitory region of TnI replaces an arginine residue at position 145 with a glycine and cosegregates with the disease. Results from several assays indicate that the inhibitory function of HCTnI(R145G) is significantly reduced. When HCTnI(R145G) was incorporated into whole troponin, Tn(R145G) (HCTnT small middle dotHCTnI(R145G) small middle dotHCTnC), only partial inhibition of the actin-tropomyosin-myosin ATPase activity was observed in the absence of Ca(2+) compared with wild type Tn (HCTnT small middle dotHCTnI small middle dotHCTnC). Maximal activation of actin-tropomyosin-myosin ATPase in the presence of Ca(2+) was also decreased in Tn(R145G) when compared with Tn. Using skinned cardiac muscle fibers, we determined that in comparison with the wild type complex 1) the complex containing HCTnI(R145G) only inhibited 84% of Ca(2+)-unregulated force, 2) the recovery of Ca(2+)-activated force was decreased, and 3) there was a significant increase in the Ca(2+) sensitivity of force development. Computer modeling of troponin C and I variables predicts that the primary defect in TnI caused by these mutations would lead to diastolic dysfunction. These results suggest that severe diastolic dysfunction and somewhat decreased contractility would be prominent clinical features and that hypertrophy could arise as a compensatory mechanism.

Adenosine Triphosphatases↗
PubMed1999

Variations in family physicians' and cardiologists' care for patients with heart failure.

BACKGROUND: Improved understanding of the reasons for underuse of diagnostic tests and treatments for congestive heart failure (CHF) may be helpful for designing future interventions to improve quality of care. METHODS: To determine differences between family physicians' and cardiologists' practice styles for diagnosis and treatment of CHF, a random sample of family physicians and cardiologists were surveyed with standardized case scenarios. RESULTS: Survey respondents were 182 family physicians and 163 cardiologists. Family physicians were less likely than cardiologists to rate measurement of left ventricular ejection fraction as "very important" for patients with new CHF, less likely to order an echocardiogram or test for ischemia, and much less likely to identify diastolic dysfunction as a cause of CHF. Family physicians were more likely to prescribe digoxin when it was not indicated (diastolic dysfunction) and less likely to prescribe digoxin and an angiotensin-converting enzyme (ACE) inhibitor when they were indicated (moderately to severely reduced left ventricular ejection fraction). Family physicians expressed more concern over the risks of ACE inhibitors in patients with blood pressure of 100/70 mm Hg or serum creatinine of 2.0 mg/dL and were less likely to prescribe an ACE inhibitor in these settings. Family physicians overestimated the risks of warfarin use for atrial fibrillation and were therefore less likely to prescribe warfarin. CONCLUSIONS: Family physicians appear to have less understanding of CHF pathophysiology (ie, systolic versus diastolic dysfunction) and how treatment differs according to the underlying disease process. Overestimation of the risk of ACE inhibitor and warfarin use may result in underprescribing these medications.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Occult restrictive hemodynamics after pediatric heart transplantation.

BACKGROUND: Although resting hemodynamics after pediatric heart transplantation are generally within normal limits, we hypothesized that occult restrictive hemodynamics suggesting diastolic dysfunction may be unmasked by acute volume loading (fluid challenge) during cardiac catheterization. We wished to determine the incidence of diastolic dysfunction and to assess whether it progressed over time. METHODS: From 1988 through 1993, a total of 100 fluid challenges were performed at the time of surveillance endomyocardial biopsy in 31 survivors of orthotopic heart transplantation. Cyclosporine-based immunosuppression was used in 16 patients, and FK506 was used in 15 patients. Right heart hemodynamics and cardiac output (thermodilution) were obtained at baseline and after a fluid challenge with 10 ml/kg of normal saline solution. The data were analyzed to determine whether type of immunosuppression or time elapsed since transplantation predicted the response to fluid challenge. RESULTS: Baseline hemodynamics were normal; however, a marked increase in atrial filling pressures occurred after fluid challenge (p < 0.001). Findings were similar in cyclosporine- and FK506-treated patients. Hemodynamic response to fluid challenge was not related to duration of time since transplantation, including studies on patients surviving more than 4 years. CONCLUSIONS: Diastolic dysfunction after heart transplantation is common; however, the abnormalities do not progress in severity, suggesting stable long-term graft function.

Adolescent↗
PubMed1997

Can the clinical examination diagnose left-sided heart failure in adults?

We systematically reviewed the literature to ascertain how well clinicians determine the probability and type of left-sided heart failure in their patients. Left-sided heart failure is characterized by decreased left ventricular ejection fraction or increased filling pressure. The type of heart failure determines optimal treatment. Systolic dysfunction exists when ejection fraction is reduced. Diastolic dysfunction is presumed to be present when filling pressure is increased with a normal ejection fraction and without another explanatory diagnosis. Many findings are associated with heart failure, and wide variation exists in clinicians' ability to detect these findings. The best findings for detecting increased filling pressure are jugular venous distention and radiographic redistribution. The best findings for detecting systolic dysfunction are abnormal apical impulse, radiographic cardiomegaly, and q waves or left bundle branch block on an electrocardiogram. Diastolic dysfunction is especially difficult to diagnose, but is associated with an elevated blood pressure during heart failure.

Clinical Competence↗
PubMed1997

Failure to maintain a low ADP concentration impairs diastolic function in hypertrophied rat hearts.

BACKGROUND: Mechanisms in addition to diastolic calcium overload may contribute to diastolic dysfunction in hypertrophied hearts. In this study, we tested the hypothesis that failure to maintain a low ADP concentration in hypertrophied hearts contributes to diastolic dysfunction by inhibiting the rate of cross-bridge cycling. METHODS AND RESULTS: By perfusing isolated rat hearts with pyruvate and 2-deoxyglucose (2DG), we were able to perturb [ADP] with minimal changes in [ATP] and [inorganic phosphate] or the contribution of glycolytic ATP to ATP synthesis. The effects of 2DG were compared in aortic-banded (LVH, n=5) and sham-operated (control, n=5) rat hearts. 31P NMR spectroscopy was used to measure the concentrations of phosphorus-containing compounds. We found a threefold increase of left ventricular end-diastolic pressure (LVEDP) in LVH during 2DG perfusion, and this increase was concomitant with a threefold increase in intracellular free [ADP]. The [ADP] in the control hearts was maintained <40 micromol/L, and no change in LVEDP was observed. A linear relationship between increases in [ADP] and LVEDP was found (r2=.66, P=.001). Furthermore, the capacity of the creatine kinase reaction, a major mechanism for maintaining a low [ADP], was decreased in LVH (P=.0001). CONCLUSIONS: Increased [ADP] contributes to diastolic dysfunction in LVH, possibly due to slowed cross-bridge cycling. Decreased capacity of the creatine kinase reaction to rephosphorylate ADP is a likely contributing mechanism to the failure to maintain a low [ADP] in LVH.

Adenosine Diphosphate↗
PubMed1999

M-mode analysis of mitral annulus motion for detection of pseudonormalization of the mitral inflow pattern.

Left ventricular (LV) diastolic dysfunction is a frequent cause of heart failure. Doppler echocardiography has become the method of choice for the noninvasive evaluation of LV diastolic dysfunction. However, pseudonormalization of mitral inflow often presents a diagnostic problem in clinical practice. We sought to define the role of mitral annulus motion in this setting. We performed echocardiography in 36 consecutive subjects (age 59 +/- 10 years). Eighteen had recently (within 3 months) been diagnosed with coronary artery disease, 18 had clinical suspicion of coronary artery disease, and 15 had symptoms of heart failure (New York Heart Association class 2.4 +/- 0.5). The amplitude (E(M)) and the slope (slope E) of early diastolic motion of the septal mitral annulus were derived from M-mode analysis. Left heart catheterization was performed for direct measurement of LV end-diastolic pressure. Pseudonormalization defined by an E/A ratio > 1 and a LV end-diastolic pressure > or = 16 mm Hg was found in 9 patients. All patients with pseudonormalization were symptomatic (New York Heart Association class 2.8 +/- 0.5). Patients with and without pseudonormalization did not differ with respect to the E/A ratio (1.29 +/- 0.44 vs 1.16 +/- 0.23, p = NS), deceleration time (182 +/- 38 vs 205 +/- 42 ms, p = NS), and isovolumic relaxation time (88 +/- 24 vs 92 +/- 18 ms, p = NS). In the group with pseudonormalization, a significant reduction of E(M) (3.9 +/- 1.6 vs 5.7 +/- 1.5 mm, p = 0.008) and slope E (24.5 +/- 11.8 vs 43.9 +/- 7.7 mm/s, p <0.001) was detected. Using E(M) <4.3 mm and slope E <35 mm/s as cut points, sensitivity and specificity for the detection of pseudonormalization were 66% and 82% for E(M) and 77% and 87% for slope E, respectively. There was no significant relation between LV end-diastolic pressure as a measure of preload and either E(M) (r = 0.44, p >0.5) or slope E (r = 0.30, p >0.2). Thus, E(M) and slope E may be preload-independent tools for assessing LV diastolic dysfunction in symptomatic patients with a pseudonormal mitral inflow pattern and elevated filling pressures.

Adult↗
PubMed2005

Cardiac alterations in cirrhosis: reversibility after liver transplantation.

BACKGROUND/AIMS: Liver cirrhosis induces cardiac alterations. We aimed to define these alterations and assess their reversibility after transplantation. METHODS: Cirrhotic patients (n = 40) and controls (n = 15) underwent echocardiography and stress ventriculography. Fifteen cirrhotics were reevaluated 6-12 months after transplantation. RESULTS: Cirrhotics had higher left ventricular wall thickness (9.6+/-1.2 vs. 8.8+/-1.2 mm; P < 0.05) and ejection fraction (73+/-6 vs. 65+/-4%, P < 0.001) than controls. Basal diastolic function was similar. During stress, cirrhotics presented lower increases of heart rate, left ventricular ejection fraction, stroke volume and cardiac index (P < 0.05 for all), and diastolic dysfunction with lower ventricular peak filling rate (P = 0.001). Exercise capacity was reduced (48+/-21 vs. 76+/-24 W; P < 0.001). Ascitic patients exhibited more diastolic dysfunction at rest and during stress compared to non-ascitic patients. Liver transplantation caused regression of ventricular wall thickness (10.2+/-1.3 vs. 9.5+/-1.2 mm; P < 0.05), improvement of diastolic function, and normalization of systolic response and exercise capacity during stress (significant increases in heart rate, ventricular ejection fraction, stroke volume and cardiac index; P < 0.05 for all). CONCLUSIONS: Cardiac alterations in cirrhosis present with mild increases in ventricular wall thickness, diastolic dysfunction that worsens with ascites and physical stress, and abnormal systolic response to stress limiting exercise capacity. Liver transplantation reverses these alterations.

Adult↗
PubMed1988

Cardiac involvement in hypertension.

Despite improved patient detection and pharmacologic therapy, the effect of treatment of hypertension on mortality from coronary artery-related events remains unresolved. Left ventricular (LV) hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. Recently, LV hypertrophy accompanying hypertension has been associated with ominous ventricular arrhythmias. However, it does not necessarily follow that regression of LV hypertrophy will reduce this increased mortality. Diastolic dysfunction, manifested by reduced ventricular distensibility of the hypertrophying left ventricle, appears to be an early characteristic of the hypertensive heart since echocardiographic techniques have demonstrated diastolic filling abnormalities in untreated essential hypertensives even before significant LV hypertrophy appears. Not all antihypertensive agents diminish LV mass and improve diastolic dysfunction. Certain sympatholytic agents, calcium antagonists, beta-adrenergic blockers, and the angiotensin-converting enzyme inhibitors appear to diminish LV hypertrophy. However, future studies are needed to determine if these agents that appear to reverse findings of LV hypertrophy and improve diastolic dysfunction will also reduce risk of coronary artery disease and related events.

Cardiomegaly↗
PubMedDate not supplied

Hyperhomocysteinaemia-induced atrial remodelling in hypertensive rats.

Studies from our laboratory and others indicate that, in addition to its purported atherothrombotic effects, hyperhomocysteinaemia (Hhe) is a powerful stimulus for ventricular remodelling, dysfunction and clinical heart failure. Because changes in atrial structure and function can impact on cardiac function in progressive ventricular remodelling and dysfunction, we conducted experiments to examine structural and functional remodelling of the atria in the hyperhomocysteinaemic hypertensive rat, a previously described model of ventricular diastolic dysfunction. Atrial muscle preparations were isolated from hearts of spontaneously hypertensive rats that were fed control, intermediate Hhe-inducing or severe Hhe-inducing diet for 10 weeks. Atrial developed tension, +dT/dt(max) and -dT/dt(max) were found to increase in parallel with levels of Hhe and ventricular diastolic dysfunction. Post-rest developed tension and the maximum developed tension observed in the presence of isoproterenol were also increased significantly in both Hhe groups compared with control. These results indicate that Hhe increases both basal and maximal contractile function in atrial muscle. Atrial structural remodelling was characterized by increased interstitial fibrosis in both Hhe groups. These data suggest that Hhe-associated changes in atrial structure and function may act to maintain ventricular filling in Hhe-induced diastolic dysfunction.

Animals↗