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PubMed1998

Relation of insulin resistance to left ventricular hypertrophy and diastolic dysfunction in obesity.

OBJECTIVE: To assess relations of left ventricular (LV) geometry and function to insulin resistance in obesity-a condition associated with volume overload and abnormal LV relaxation. DESIGN: Cross-sectional relational study. SUBJECTS: 27 healthy overweight-obese subjects (18 women, body mass index (BMI) = 35.0+/-4.0 kg/m2) and 31 age-matched normal-weight controls (21 women, BMI = 22.6+/-2.4 kg/m2). MEASUREMENTS: Subjects were studied by Doppler-echocardiography the same day and hour (08.00 h) as measurements of fasting insulin and blood glucose were made. Insulin resistance was determined by the 'Homeostasis Assessment Model'. RESULTS: Twelve obese subjects with insulin resistance (IR) had higher body size than 15 patients without IR and higher blood pressure than normal-weight controls (all P < 0.01). Relative IR was related to isovolumic relaxation time. This relation was not maintained after controlling for age, blood pressure, weight and height. Isovolumic relaxation time was, however, positively related to diastolic blood pressure, a measure of load, in normal controls (r=0.44) and obese without IR (r=0.62) but not in insulin resistant subjects (r=0.14). CONCLUSION: IR does not independently influence myocardial relaxation in uncomplicated obesity, but modulates the effect of load on active diastole.

Adult↗
PubMed1999

Left ventricular diastolic dysfunction in patients with subclinical hypothyroidism.

Although subclinical hypothyroidism is frequently diagnosed, the decision to institute a substitutive therapy with L-T4 remains controversial. Because the cardiovascular system is considered a main target for the action of thyroid hormone, we investigated whether subclinical hypothyroidism induces cardiovascular abnormalities. Twenty-six patients (mean age, 36 +/- 12 yr) were evaluated by Doppler-echocardiography, whereas a subgroup of 10 patients, randomly selected, were reevaluated after 6 months of L-T4 substitutive therapy (mean dose, 68 microg daily). Thirty subjects (matched for age, sex, and body surface area) served as controls. Mean plasma TSH was significantly higher in patients (P < 0.001), whereas mean serum free T4 and free T3 concentrations, although in the normal range, were significantly lower (P < 0.001 and P < 0.005, respectively). Blood pressure and heart rate did not differ from control values. Echocardiogram examination showed no abnormalities of the left ventricular morphology and a slight, but not significant, reduction in the systolic function in the patient group. In contrast, Doppler-derived indices of diastolic function showed significant prolongation of the isovolumic relaxation time (94 +/- 13 vs. 84 +/- 8 msec; P < 0.001), increased A wave (55 +/- 13 vs. 48 +/- 9 cm/sec; P < 0.05), and reduced early diastolic mitral flow velocity/late diastolic mitral flow velocity ratio (1.4 +/- 0.3 vs. 1.7 +/- 0.3; P < 0.001). In the subgroup of 10 patients, thyroid hormone profile was normalized by 6 months of L-T4 substitutive therapy, whereas no changes were observed in the left ventricular morphology. Systolic function was significantly enhanced, as compared with pretreatment values (P < 0.01) but did not differ from control values. Also, systemic vascular resistance was significantly decreased by L-T4 replacement therapy. Assessment of diastolic function showed significant shortening of isovolumic relaxation time (77 +/- 15 vs. 91 +/- 8; P < 0.05), reduction of A wave (51 +/- 13 vs. 60 +/- 12; P < 0.01), and increase of early diastolic mitral flow velocity/late diastolic mitral flow velocity ratio (1.7 +/- 0.4 vs. 1.3 +/- 0.3; P < 0.001). These indices, however, were comparable with those of control subjects. These findings indicate that subclinical hypothyroidism affects diastolic function and that this abnormality may be reversed by L-T4 substitutive therapy.

Adult↗
PubMed2001

Right ventricular myocardial diastolic dysfunction in different kinds of cardiac hypertrophy: analysis by pulsed Doppler tissue imaging.

BACKGROUND: Right ventricular (RV) chamber involvement has been demonstrated in hypertrophic cardiomyopathy (HCM) as well as in hypertensive left ventricular hypertrophy (LVH) but little is known about RV myocardial dysfunction occurring in these two pathologies. The aim of this study was to compare Doppler tissue imaging (DTI) of the right ventricle in HCM and LVH in relation to DTI of the left ventricle and Doppler standard of the RV and left ventricular (LV) inflow. METHODS: Thirty controls, 20 hypertensives with LVH, and 23 patients with HCM involving the interventricular septum underwent Doppler echocardiography and pulsed DTI of the LV lateral mitral annulus and the RV lateral tricuspid annulus. RESULTS: Patients with HCM had a higher blood pressure, septal thickness and LV mass in comparison with the other two groups. The RV wall thickness did not differ between HCM and LVH. The fractional shortening, but not the tricuspid annular plane excursion, was higher in HCM. After adjusting for the mean blood pressure, the Doppler-derived global LV and RV diastolic functions were more impaired in HCM than in LVH. Also the majority of DTI LV and RV diastolic measurements were altered more in HCM. At the RV tricuspid annulus, myocardial diastolic indexes were impaired in HCM and LVH in comparison with controls but the deceleration and relaxation times distinguished also HCM and LVH, being much longer in HCM (p < 0.0001). In the overall population, the RV myocardial relaxation time was positively related to the septal wall thickness and the RV wall thickness, even after adjusting for age, heart rate, diastolic blood pressure, fractional shortening and DTI mitral relaxation time. CONCLUSIONS: The impairment of RV myocardial relaxation is much more evident in HCM than in LVH, its degree being independently associated with the extent of both the septal and RV wall thickness. Pulsed DTI may be useful to distinguish the extent of RV myocardial dysfunction in different types of cardiac hypertrophy.

Adult↗
PubMed2001

Left ventricular diastolic dysfunction in patients with bronchial asthma with long-term oral beta2-adrenoceptor agonists.

BACKGROUND: Long-term administration of oral beta(2)-adrenergic receptor agonists (beta(2)-AG) in patients with bronchial asthma (BA) causes disastrous events such as sudden death and heart attack. However, long-term effects of beta(2)-AG on cardiac function have not been previously quantified. METHODS: Seventy-four patients with BA with regular long-term use of oral beta(2)-AG (group A) and 69 patients with BA without beta(2)- AG (group B) were examined in medical records of outpatient clinics from 1985 to 1999. In the prospective study, echocardiography was performed in 48 consecutive patients from January to April 1999. There were 26 patients with regular oral use of beta(2)-AG (group a) and 22 patients without beta(2)-AG (group b). Twenty-one age-matched normal volunteers without heart or pulmonary diseases were used as control subjects (group c). Oral beta(2)-AG was withdrawn from remedies in 11 patients of group a, and echocardiographic studies were repeated 2 weeks after its cessation. RESULTS: Events related to heart failure were more frequently seen in group A than in group B (14% vs 1%, P <.01). The echocardiographic study showed that indexes of left ventricular diastolic but not systolic function were significantly deteriorated in group a, along with a markedly reduced level of plasma norepinephrine concentration (P <.05 vs groups b and c). When heart rate was adjusted to 90 beats/min during isoproterenol infusion, left ventricular diastolic function remained deteriorated in group a (P <.05 vs groups b and c). In 11 patients of group a, the cessation of beta(2)-AG for 2 weeks resulted in an improvement of left ventricular diastolic function and in an increase of plasma norepinephrine level (P <.01). CONCLUSIONS: Long-term use of oral beta(2)-AG impaired left ventricular diastolic function in patients with BA, and the cessation of beta(2)-AG reversed diastolic pump performance to the normal level.

Administration, Oral↗
PubMed2006

Diastolic dysfunction and abnormality of the Na+/Ca2+ exchanger in single uremic cardiac myocytes.

Cardiovascular disease is the most common cause of death in patients with end-stage renal disease, possibly due to a specific "uremic cardiomyopathy". This study investigated the function of the Na(+)/Ca(2+) exchanger in single cardiac myocytes from a model of early renal impairment. Mild uremia was induced by partial (5/6) nephrectomy in male Wistar rats. After 4 weeks, ventricular myocytes were isolated, loaded with the fluorescent Ca(2+) indicator indo-1, and contractile function and calcium transients recorded following electrical pacing at 0.2 Hz. Relaxation from rapid cooling contractures (RCCs) was also studied. Cells from uremic animals (U) were hypertrophied compared with controls (C), with a significant increase in width (14%; P<0.02) and cross-sectional area (13%; P<0.03). There was a significant increase in diastolic intracellular Ca(2+) ratio in the uremic cells (C, 0.33+/-0.00 vs U, 0.37+/-0.02; P<0.02), although the amount of calcium released per twitch was similar. Uremic cells were slower to relax following RCCs, however when Na(+)/Ca(2+) exchange was inhibited using a Na(+)-free/Ca(2+)-free solution, this difference was abolished. Under these conditions, there was little difference in the relaxation rate of control cells, indicating that the Na(+)/Ca(2+) exchanger plays only a minor role in relaxation in normal rat myocytes. However in uremia, the data indicate that the Na(+)/Ca(2+) exchanger actively interfered with relaxation, possibly by working in reverse rather than forward mode. These results indicate that myocyte relaxation and Ca(2+) handling are abnormal in early uremia and may provide further evidence for the existence of a specific "uremic cardiomyopathy".

Animals↗
PubMed1993

Sarcoplasmic reticulum calcium mobilization in right ventricular pressure-overload hypertrophy in the ferret: relationships to diastolic dysfunction and a negative treppe.

In a model of right-ventricular pressure-overload hypertrophy (POH) in the ferret, action potential duration (to 90% repolarization) was found to be significantly longer (228 +/- 11 vs 314 +/- 12 ms) with no change in amplitude (85 +/- 3 vs 85 +/- 2 mV) or resting membrane potential (-79 +/- 1.5 vs -79 +/- 1 mV) for control and POH, respectively. Peak sarcoplasmic reticulum Ca2+ release (expressed as the logarithm of the fractional luminescence, -4.2 +/- 0.1 vs -4.4 +/- 0.3) and resting calcium concentrations (-5.5 +/- 0.1 vs -5.7 +/- 0.1) were not different between the two groups (control vs POH respectively). Muscles from control and POH animals demonstrated a positive force/interval relationship in the presence of physiological extracellular [Ca2+]. However, unlike muscles from control animals, muscles from animals with POH subjected to increasing frequencies of contraction in the presence of increased extracellular [Ca2+] demonstrated further impairment of diastolic relaxation and a negative treppe. Exposure of muscles from POH animals to isoproterenol returned the slowed Ca2+ uptake by the sarcoplasmic reticulum as detected with aequorin to control values, although the relaxation phase of the isometric twitch remained prolonged compared to non-hypertrophied muscles. Exposure to milrinone also abbreviated the time course of the intracellular Ca2+ transient, but did not return it to that seen in normal myocardium. The exposure of non-hypertrophied isolated muscles to caffeine resulted in similar prolongation of the isometric twitch duration to that seen in hypertrophied myocardium. Results of these experiments suggest that impaired muscle relaxation in POH reflects changes at the level of the myofilaments. Thus, although slowed intracellular calcium mobilization contributes to diastolic relaxation abnormalities, it can not be the sole factor responsible for the slowed relaxation as has been suggested.

Action Potentials↗
PubMed1991

Protective effect of increased glycolytic substrate against systolic and diastolic dysfunction and increased coronary resistance from prolonged global underperfusion and reperfusion in isolated rabbit hearts perfused with erythrocyte suspensions.

Current therapy of myocardial infarction may include early reperfusion. We simulated myocardial perfusion conditions during evolving myocardial infarction in isolated, normothermic, isovolumic rabbit hearts perfused with buffer containing bovine red blood cells (hematocrit of 40%), and we assessed the effects of high levels of glucose and insulin as "therapy" during prolonged (150-minute) severe underperfusion and reperfusion. Protocol 1 consisted of underperfusion at a constant coronary perfusion pressure of 8 mm Hg. The control group (n = 8) received 5.5 mmol/l glucose and 15 microunits/ml insulin; the group treated with high levels of glucose and insulin (G + I) (n = 8) received 19.5 mmol/l glucose and 250 microunits/ml insulin during both underperfusion and reperfusion. Relative to the control group, the G + I group experienced 1) greater developed pressure during underperfusion and increased recovery during reperfusion, 2) preserved diastolic function during underperfusion and reperfusion, 3) lower coronary resistance and greater coronary flow during the underperfusion period, 4) increased glycolytic flux and preserved glycogen stores and high energy phosphate levels, and 5) less loss of myocyte enzymes (creatine kinase and alanine aminotransferase). In protocol 2, coronary flow was kept identical in control (n = 8) and G + I hearts (n = 8) during the underperfusion period, and left ventricular end-diastolic pressure was kept below 10 mm Hg in both groups to minimize subendocardial damage and vascular compression. In this protocol, the effect of the G + I intervention in the prevention of an increase in coronary resistance during the underperfusion period was distinguished from its myocellular metabolic effects; the high G + I substrate had protective effects on mechanical and metabolic function that were less marked than, but similar to, those in protocol 1, indicating that its mechanisms of protection during underperfusion affected both cardiac function and coronary resistance. We conclude that the G + I intervention, in clinically relevant concentrations, markedly protected severely underperfused myocardium for 150 minutes and may be a beneficial intervention in combination with reperfusion therapy in acute myocardial infarction.

Animals↗
PubMed1990

Sepsis-induced diastolic dysfunction in chronic canine peritonitis.

A chronic canine model of hyperdynamic sepsis was achieved by cecal ligation and puncture (SEP) in conjunction with continuous high-volume fluid resuscitation. Cardiac function was evaluated using ultrasonic cardiac crystals placed across the major, minor, and wall thickness axes of the left ventricle, together with simultaneous arterial and ventricular pressure measurement. Seven to 10 days after crystal implantation, animals were randomized to either SEP (n = 10) or sham laparotomy control (n = 7). SEP dogs became febrile and lethargic, with elevated leukocyte counts and positive blood cultures for enteric organisms. They were also hyperdynamic, with significant increases in heart rate and cardiac output and a fall in systemic vascular resistance. Systolic blood pressure, stroke volume, and ejection fraction remained stable. Relative to control, the SEP group demonstrated a significant reduction in intrinsic contractility during systole, as measured by the heart rate and load-independent index of left ventricular performance Emax (P less than 0.01), confirming the observations of others. In addition, however, diastolic function also became markedly abnormal with a progressive increase in unstressed and end-diastolic ventricular volumes (P less than 0.05) and a significant decrease in myocardial compliance as quantitated by transmural pressure vs. volume-strain analysis. It is hypothesized that this increase in diastolic volume helps to maintain global cardiac performance during the hyperdynamic response to sepsis in the presence of adequate volume support.

Animals↗
PubMed1990

Clinical experience of therapy with xamoterol in patients with severe systolic and diastolic dysfunction.

Xamoterol ('Corwin', 'Carwin', 'Corwil', 'Xamtol', ICI118, 587)*, a partial beta-agonist, has beneficial effects in patients with mild to moderate heart failure. In acute haemodynamic studies in more severe heart failure some patients have shown negative inotropic and chronotropic effects, although treatment with a partial agonist should protect the heart against excessive stimulation, while providing a baseline level of sympathetic drive. This study examined the effects of oral xamoterol in patients with moderate to severe heart failure. Ten patients were studied, nine with ischaemic heart disease. All but one were in New York Heart Association (NYHA) functional Class III. Other treatment, including angiotensin converting enzyme (ACE) inhibitors, was continued. The patients underwent a standard bicycle exercise test, and the following day cardiac catheterization was performed to obtain measurements of ventricular size (by cineangiography) and pressures during the cardiac cycle. The patients began treatment with xamoterol 200 mg b.d. in addition to their baseline therapy, and this was continued for an average of 9 weeks, after which the exercise test and the haemodynamic investigations were repeated. At baseline, all patients had a raised left ventricular end-diastolic pressure (LVEDP) and nine had a low election fraction, raised end-systolic and end-diastolic volume indices and reduced left ventricular (+) dP/dtmax Xamoterol produced a marked reduction in left ventricular filling pressure, a fall in end-systolic volume index and improvements in T1, (+) dP/dtmax and (dP/dt)/DP40 with no change in mean aortic pressure. Duration of exercise increased in four patients, and did not change in the other four tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1999

Insulin and diastolic dysfunction in lean and obese hypertensives: genetic influence.

We investigated the influence of genetic predisposition to hypertension by studying the relation between insulin sensitivity and left ventricular (LV) mass and function in untreated lean and obese hypertensives. We selected 50 lean hypertensives with normotensive parents (negative family history of hypertension [F-]), 64 lean hypertensives with 1 or both parents hypertensive (positive family history of hypertension [F+]), 40 obese F- hypertensives, and 43 obese F+ hypertensives. The 4 groups were comparable regarding age, gender, 24-hour blood pressure profile, and known duration of hypertension. We measured glucose, insulin, and C-peptide during fasting and during an oral glucose tolerance test; LV morphology and function were assessed by digitized M-mode echocardiography. Glucose (fasting and test) levels were normal in all and similar among the 4 groups. Insulin and C-peptide (fasting and stimulated) levels were higher in obese hypertensives than in lean hypertensives; at similar body mass index, insulin and C-peptide levels were higher in F+ than in F- groups. Compared with lean hypertensives, obese hypertensives had greater LV mass index; LV systolic function was normal in all and similar among the groups. The indices of LV diastolic function were significantly lower in F+ than in F- groups. LV mass index did not correlate with metabolic parameters; the indices of LV diastolic function were inversely correlated with insulin area during test in only the 2 F+ groups. In conclusion, genetic predisposition to hypertension is associated with a reduced insulin sensitivity and affects the response of the myocardium to increased insulin levels, inducing a greater impairment of diastolic function. Insulin sensitivity and genetic predisposition to hypertension seem to have no influence on LV mass.

Adult↗
PubMed1991

Symptom-limited exercise testing causes sustained diastolic dysfunction in patients with coronary disease and low effort tolerance.

Exercise stress testing is routinely used for the noninvasive assessment of coronary artery disease and is considered a safe procedure. However, the provocation of severe ischemia might potentially cause delayed recovery of myocardial function. To investigate the possibility that maximal exercise testing could induce prolonged impairment of left ventricular function, 15 patients with angiographically proved coronary disease and 9 age-matched control subjects with atypical chest pain and normal coronary arteries were studied. Radionuclide ventriculography was performed at rest, at peak exercise, during recovery and 2 and 7 days after exercise. Ejection fraction, peak filling and peak emptying rates and left ventricular wall motion were analyzed. All control subjects had a normal exercise test at maximal work loads and improved left ventricular function on exercise. Patients developed 1 mm ST depression at 217 +/- 161 s at a work load of 70 +/- 30 W and a rate-pressure product of 18,530 +/- 4,465 mm Hg x beats/min. Although exercise was discontinued when angina or equivalent symptoms occurred, in all patients diagnostic ST depression (greater than or equal to 1 mm) developed much earlier than symptoms. Predictably, at peak exercise patients showed a decrease in ejection fraction and peak emptying and filling rates. Ejection fraction and peak emptying rate normalized within the recovery period, whereas peak filling rate remained depressed throughout recovery (p less than 0.002) and was still reduced 2 days after exercise (p less than 0.02). In conclusion, in patients with severe impairement of coronary flow reserve, maximal exercise may cause sustained impairement of diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Normalized left ventricular filling indexes to detect diastolic dysfunction in hypertension and in hypertrophic cardiomyopathy.

In order to establish a normalizing method for left ventricular filling indexes, peak filling rate (PFR) and time to peak filling rate (TPFR), derived from resting radionuclide ventriculography using Fourier analysis with third-order harmonics, were analyzed in 45 normal subjects, 40 hypertensive patients, and 29 patients with hypertrophic cardiomyopathy. PFR was significantly negatively correlated with age (r = -0.62) and significantly positively correlated with peak ejection rate (PER) (r = 0.58) in normals. TPFR normalized for heart rate (N-TPFR) was correlated positively with age in normals (r = 0.60) and hypertensives (r = 0.49) but not in patients with hypertrophic cardiomyopathy. N-TPFR was not significantly correlated with systolic parameters. A significant relationship between PFR normalized to PER (PFR/PER) and age was observed in normals (r = -0.58) but not in patients with hypertension or hypertrophic cardiomyopathy. To cancel the ageing effect, individual data of PFR/PER and N-TPFR were expressed as a percentage of the predicted regression value in normal subjects (%PFR/PER and %N-TPFR, respectively). Per cent PFR/PER was significantly lower and %N-TPFR was significantly greater in patients with hypertension and hypertrophic cardiomyopathy compared to normals. When normal limits of these indexes were defined as %PFR/PER greater than 80% and %N-TPFR less than 120%, the sensitivity, specificity and diagnostic accuracy of differentiating normals from patients with hypertension or hypertrophic cardiomyopathy were 41 of 45 (91%), 44 of 68 (65%), and 85 of 113 (75%), respectively. These findings indicate that %PFR/PER and %N-TPFR might be more reasonably normalized parameters for describing diastolic filling and its abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2002

Use of HIV protease inhibitors is associated with left ventricular morphologic changes and diastolic dysfunction.

HIV protease inhibitor (PI) therapy may be associated with cardiac and vascular complications. We assessed the effects of PIs on cardiac function and structure. M-mode, cross-sectional, and Doppler echocardiography were performed in 98 consecutive black adults aged 25 to 45 years with HIV infection who were receiving antiretroviral therapy. Forty-five (56.1%) took PIs (mean duration of PI use: 29.6 +/- 12.2 months). No significant differences between the PI and non-PI groups were found in left ventricular (LV) systolic function and cardiac valve regurgitation. Those who took PIs had a significantly higher interventricular septum thickness (1.1 +/- 0.3 vs. 1.0 +/- 0.2 cm; p =.049), LV posterior wall thickness (1.1 +/- 0.2 vs. 1.0 +/- 0.2; p =.027), and lower ratio of early peak velocity (E wave) to late peak velocity (A wave) (E/A ratio) (1.36 +/- 0.30 vs. 1.53 +/- 0.31; p =.023) than did those who did not take PIs. Linear regression analyses indicated that posterior wall thickness, septum thickness, left atrial dimension, LV mass, and E/A ratios were significantly associated with the log-transformed duration of PI therapy. Despite the proven benefits of PIs in patients with HIV infection, this report demonstrates an association between continued PI intake and LV hypertrophy that should be known and taken into consideration in the analysis of cardiac structure and function in patients with HIV infection.

Adult↗
PubMed2006

Metallothionein prolongs survival and antagonizes senescence-associated cardiomyocyte diastolic dysfunction: role of oxidative stress.

Senescence is accompanied by oxidative stress and cardiac dysfunction, although the link between the two remains unclear. This study examined the role of antioxidant metallothionein on cardiomyocyte function, superoxide generation, the oxidative stress biomarker aconitase activity, cytochrome c release, and expression of oxidative stress-related proteins, such as the GTPase RhoA and NADPH oxidase protein p47phox in young (5-6 mo) and aged (26-28 mo) FVB wild-type (WT) and cardiac-specific metallothionein transgenic mice. Metallothionein mice showed a longer life span (by approximately 4 mo) than FVB mice evaluated by the Kaplan-Meier survival curve. Compared with young cardiomyocytes, aged myocytes displayed prolonged TR(90), reduced tolerance to high stimulus frequency, and slowed intracellular Ca2+ decay, all of which were nullified by metallothionein. Aging increased superoxide generation, active RhoA abundance, cytochrome c release, and p47phox expression and suppressed aconitase activity without affecting protein nitrotyrosine formation in the hearts. These aging-induced changes in oxidative stress and related protein biomarkers were attenuated by metallothionein. Aged metallothionein mouse myocytes were more resistant to the superoxide donor pyrogallol-induced superoxide generation and apoptosis. In addition, aging-associated prolongation in TR90 was blunted by the Rho kinase inhibitor Y-27632. Collectively, our data demonstrated that metallothionein may alleviate aging-induced cardiac contractile defects and oxidative stress, which may contribute to prolonged life span in metallothionein transgenic mice.

Aconitate Hydratase↗