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PubMed2002

Is left ventricular hypertrophy a risk factor in hypertensive patients?

BACKGROUND: Left ventricular hypertrophy (LVH) is supposed to be a risk factor of cardiovascular (CV) complications in hypertensive patients. AIM: To compare clinical events in hypertensives with and without LVH. PATIENTS AND METHODS: 319 hypertensives with LVH (mean age 64.1+/-10.6 ys) and 177 hypertensives without LVH (mean age 62.5+/-11.3 ys). LVH defined by echo Penn convention as left ventricular mass index >134 g/m2 in men and >110 g/m2 in women. Clinical events--heart failure (EF<40 %), left ventricular diastolic dysfunction (echo-doppler: transmitral-flow where peak A>peak E), myocardial infarction (history, ECG, cardiac enzymes), chronic atrial fibrillation (more than 2 weeks duration), mitral regurgitation (echo) and renal involvement (creatininemia>120 micromol/l). The two groups of hypertensives were matched by demographic criteria, duration and intensity of hypertension, obesity, diabetes mellitus, lipid serum levels and smoking habits. RESULTS: There were statistically significant at least p<0.05 more CV events (heart failure, left ventricular diastolic dysfunction, myocardial infarction, chronic atrial fibrillation, and mitral regurgitation cases) and renal involvement in LVH-positive patients than in LVH-negative patients. CONCLUSION: LVH is a strong risk factor for clinical events in hypertensives, which necessitates their more intensive treatment, mainly with drugs producing also LVH regression. (Tab. 5, Ref. 48.)

Female↗
PubMed2006

Left atrial emptying fraction correlation with vascular pedicle width in patients with normal systolic function.

OBJECTIVE: To determine the correlation and diagnostic utility of impaired left atrial emptying fraction, an indicator of diastolic dysfunction, with raised intravascular volume determined by vascular pedicle width on upright postero-anterior chest roentgenogram. DESIGN: Cohort study. PLACE AND DURATION OF STUDY: Department of Medicine, King Abdulaziz National Guard Hospital, Alhasa, Saudi Arabia from October till December 2002. PATIENTS AND METHODS: Thirty-two out of 56 patients with normal systolic function (ejection fraction >50%) on echocardiogram were included in the study. Left atrial dimensions were measured at the end of left ventricular diastole (LADed) and systole (LADes) on M-mode tracing. Left atrial emptying fraction (LAEF) was calculated by dividing LADed by LADes. Ratio of peak early diastolic velocity (E/A) to peak late diastolic velocity, isovolemic relaxation time (IVRT) and deceleration time of E-wave (DT) were also recorded on transmitral Doppler signal. Postero-anterior views of chest X-rays done within 48 hours of echocardiogram were studied for the measurement of vascular pedicle width (VPW) and cardiothoracic ratio (CTR). Univariate and multiple regression analysis were performed to identify possible predictors of VPW. Receiver operator curves were constructed to see diagnostic utility of impaired LAEF for raised intravascular volume measured by VPW. RESULTS: Mean age for the patients was 58.56 +/- 17 years. There were 15 females (46.9%) and 17 males (54.1%). LADes, LADed, LAEF and DT were 2.89 +/- 0.63 cm, 3.81 +/- 0.53 cm, 0.75 +/- 0.10 and 202 +/- 49.9 msec respectively. VPW and CTR were 55.81 +/- 10.2 mm and 0.54 +/- 0.08. Significant independent predictors of VPW on univariate regression analysis were entered into multiple regression models, which revealed LAEF and DT as the only predictors of VPW. The final regression equation was VPW = 15.43 + 35.7 (LAEF) + 0.06 (DT), R2 = 0.35, p = 0.0008. LAEF > 0.75 had a sensitivity of 74% and specificity of 94% for diagnosing raised intravascular volume defined as VPW > 53 mm. CONCLUSION: LAEF > 0.75 is a reliable indicator of intravascular volume expansion in patients with normal systolic function signifying diastolic dysfunction and activation of salt and water retaining mechanisms.

Atrial Function, Left↗
PubMed2002

[Retrospective study of hospitalizations for heart failure in elderly patients in a cardiology service of a general hospital center].

The results of a retrospective study of patients over 70 years of age admitted to the cardiology department of Meaux Hospital for cardiac failure in 1997 are reported. The cases of 143 patients were analysed with respect to two age groups: 70-79 years, and over 80 years of age. The principal aetiology of cardiac failure in all ages was ischaemic heart disease. Hypertensive heart disease was observed in younger patients and valvular heart disease in the more elderly. No significant gender differences were observed in those affected by this pathology or by left ventricular systolic or diastolic dysfunction between the younger and older patients, men having more systolic dysfunction than women. The main causal factor of decompensation in all ages was supraventricular arrhythmias. From the therapeutic point of view, the prescription of ACE inhibitors was relatively common but at low doses. Re-hospitalisation for cardiac failure was common and observed mainly in patients with low ejection fractions. The average hospital stay was 12.58 days. The hospital mortality was high: 15%. Two year survival was 41% with no difference between patients with systolic or diastolic dysfunction. Pluridisciplinary management should reduce the number of re-hospitalisation, improve the quality of life and, perhaps, improve survival.

Age Factors↗
PubMed2002

Changes in titin isoform expression in pacing-induced cardiac failure give rise to increased passive muscle stiffness.

BACKGROUND: Titin contains a molecular spring segment that underlies passive myocardial stiffness. Myocardium coexpresses titin isoforms with molecular spring length variants and, consequently, distinct stiffness characteristics: the stiff N2B isoform (short spring) and more compliant N2BA isoform (long spring). We tested whether changes in titin isoform expression occur in the diastolic dysfunction that accompanies heart failure. METHODS AND RESULTS: We used the tachycardia-induced dilated cardiomyopathy canine model (4-week pacing) and found that control myocardium coexpresses the N2B and N2BA isoforms at similar levels, whereas in dilated cardiomyopathy the expression ratio had shifted, without affecting the amount of total titin, toward more prominent N2B expression. This shift was accompanied by elevated titin-based passive muscle stiffness. Pacing also resulted in significant upregulation of obscurin, an approximately 800-kDa elastic protein with several signaling domains. CONCLUSIONS: Coexpression of titin isoforms with distinct mechanical properties allows modulation of passive stiffness via adjustment of the isoform expression ratio. The canine pacing-induced heart failure model uses this mechanism to increase myocardial stiffness. Thus, changes in titin isoform expression may play a role in diastolic dysfunction in heart failure.

Animals↗
PubMedDate not supplied

Pathophysiology of heart failure: changing perceptions.

Heart failure occurs when myocardial muscle dysfunction prevents the heart from pumping enough blood at normal cardiac pressures to meet the metabolic needs of the body, especially during exercise, and compensatory hemodynamic and neurohormonal mechanisms are overwhelmed or maladaptive. Pathologic classifications are broadly based on the presence of systolic dysfunction (dilated cardiomyopathy) and diastolic dysfunction (hypertrophic or restrictive cardiomyopathies). Coronary artery disease, idiopathic dilated cardiomyopathy, and hypertension are the most frequent causes, and myocardial function may be impaired by some drugs. When contractility is reduced, stroke volume and cardiac output are decreased, and alterations in the kidneys may induce fluid retention to compensate for the perceived low output and reduced circulating blood volume. Fluid retention, in turn, causes increased preload or filling pressure and symptoms of pulmonary congestion. Depressed contractility also results in a reduction in blood pressure, leading to compensatory neurohormonal activation and vasoconstriction, which significantly elevate afterload, further reduce stroke volume, and lead to deleterious cardiac remodeling. The overall clinical approach includes defining the etiology, identifying precipitant factors, and assessing the severity of myocardial dysfunction and clinical symptoms.

Cardiac Output, Low↗
PubMed2001

The pathogenesis of acute pulmonary edema associated with hypertension.

BACKGROUND: Patients with acute pulmonary edema often have marked hypertension but, after reduction of the blood pressure, have a normal left ventricular ejection fraction (> or =0.50). However, the pulmonary edema may not have resulted from isolated diastolic dysfunction but, instead, may be due to transient systolic dysfunction, acute mitral regurgitation, or both. METHODS: We studied 38 patients (14 men and 24 women; mean [+/-SD] age, 67+/-13 years) with acute pulmonary edema and systolic blood pressure greater than 160 mm Hg. We evaluated the ejection fraction and regional function by two-dimensional Doppler echocardiography, both during the acute episode and one to three days after treatment. RESULTS: The mean systolic blood pressure was 200+/-26 mm Hg during the initial echocardiographic examination and was reduced to 139+/-17 mm Hg (P< 0.01) at the time of the follow-up examination. Despite the marked difference in blood pressure, the ejection fraction was similar during the acute episode (0.50+/-0.15) and after treatment (0.50+/-0.13). The left ventricular regional wall-motion index (the mean value for 16 segments) was also the same during the acute episode (1.6+/-0.6) and after treatment (1.6+/-0.6). No patient had severe mitral regurgitation during the acute episode. Eighteen patients had a normal ejection fraction (at least 0.50) after treatment. In 16 of these 18 patients, the ejection fraction was at least 0.50 during the acute episode. CONCLUSIONS: In patients with hypertensive pulmonary edema, a normal ejection fraction after treatment suggests that the edema was due to the exacerbation of diastolic dysfunction by hypertension--not to transient systolic dysfunction or mitral regurgitation.

Acute Disease↗
PubMed2006

Cardiac overexpression of alcohol dehydrogenase (ADH) alleviates aging-associated cardiomyocyte contractile dysfunction: role of intracellular Ca2+ cycling proteins.

Aging is a complex biological process with contributions from a wide variety of genes including insulin-like growth factor I and alcohol dehydrogenase (ADH), which decline with advanced age. The goal of this study was to examine if ADH enzyme plays any role in cardiac aging. Ventricular myocytes were isolated from young (2-3 months old) or aged (26-28 months old) male FVB wild-type and cardiac-specific ADH (class I, isozyme type 1) transgenic mice. Mechanical properties were measured using an IonOptix system. Aged FVB myocytes displayed significantly reduced ADH activity compared with young ones, which was restored by the ADH transgene. Compared with young cardiomyocytes, aged FVB myocytes exhibited prolonged relengthening duration and a steaper decline in peak shortening amplitude in response to elevated electrical stimuli. Although ADH transgene itself did not alter mechanical properties in young mice, it rescued aging-associated diastolic dysfunction without affecting dampened contractile response to high stimulus frequency. Immunoblot analysis revealed reduced sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a) and Na(+)-Ca(2+) exchanger (NCX) levels in conjunction with enhanced phospholamban expression in aged FVB hearts. ADH transgene prevented aging-induced reduction in SERCA2a and NCX without affecting up-regulated phospholamban. Our data suggest that aging is associated with a reduced ADH enzymatic activity and diastolic dysfunction, which may be corrected with cardiac overexpression of the ADH enzyme. Alteration in cardiac Ca(2+) cycling proteins including SERCA2a and NCX may play a role in both pathogenesis of cardiac aging and the beneficial effect of ADH enzyme.

Aging↗
PubMed2004

Early carotid atherosclerosis and cardiac diastolic abnormalities in hypertensive subjects.

Despite the fact that it is known that hypertension may be associated to early atherosclerosis manifestations, few data are to date available on the relationship between early carotid abnormalities and left ventricular diastolic dysfunction. To address this issue, 142 hypertensive patients (64 females and 78 males) younger than 55 years, at the first diagnosis of mild-to-moderate essential hypertension (WHO/ISH criteria), were selected from a database consisting of 3541 subjects referred to ultrasound cardiovascular laboratory in the last 5 years. Carotid intima-media thickness (IMT) was detected by high-resolution vascular ultrasound and left ventricular structure and function by the use of Doppler echocardiography. According to carotid IMT values, all patients were subgrouped into two groups consisting of 89 (62.6%) pts with IMT > or = 1 mm (A) and 53 (37.4%) pts with IMT < 1 mm (B). Our results show that isovolumic relaxation time (IVRT), deceleration time of E velocity (EDT) and left ventricular relative wall thickness (LV-RWT) were significantly (P < 0.05) higher in group A (IVRT 112 +/- 8.9 ms; EDT 288 +/- 21.8 ms; LV-RWT 0.40 +/- 0.08) than in group B (IVRT 92.3 +/- 4.6 ms; EDT 203.3 +/- 27.01 ms; LV- RWT 0.37 +/- 0.06). Moreover, the prevalence of left ventricular hypertrophy (LVH) was significantly (P < 0.01) higher in group A (30/89; 33.7%) than in group B (8/53; 15%). A positive correlation (P < 0.001) between IMT, EDT and IVRT was found only in hypertensives without LVH. These results are consistent with the indication that IMT evaluation has to be recommended both in hypertensive patients with LVH and in those without LVH, but with left ventricular diastolic dysfunction. This approach might improve the prognostic stratification of hypertensive subjects and it might be suitable to recognize the subset of patients at a higher risk of cardiovascular disease or events early.

Adult↗
PubMed1997

Effects and interactions of nitrous oxide, myocardial ischemia, and reperfusion on left ventricular diastolic function.

The effects of nitrous oxide on left ventricular diastolic function and its potential interactions with ischemia-induced diastolic dysfunction have not been described. Accordingly, we investigated the effects of nitrous oxide in ischemic and remote nonischemic myocardium during baseline, 90 min severe low-flow myocardial ischemia (systolic bulge), and reperfusion in 11 open-chest dogs. Anesthesia was maintained with fentanyl infusion (2 micrograms.kg-1.min-1), animals were ventilated with 60% nitrogen in oxygen, and hemodynamic variables were recorded prior to and after the replacement of nitrogen by 60% nitrous oxide. During baseline, nitrous oxide moderately increased chamber stiffness (+ 10%), myocardial stiffness (+33%), and unstressed length (+4%) and decreased the peak lengthening rate (-10%). Moreover, nitrous oxide decreased regional contractility during baseline (-12% at apex, -8% at base) as well as in nonischemic myocardium during myocardial ischemia (-9%) and reperfusion (-8%). However, nitrous oxide did not modify ischemia-induced systolic or diastolic dysfunction in ischemic myocardium during ischemia and reperfusion. Myocardial ischemia (+45%) and reperfusion (+57%) were associated with an increase in myocardial stiffness of nonischemic myocardium regardless of the anesthetic technique used. This study is the first to demonstrate that in addition to its well established negative inotropic effect, nitrous oxide affects regional diastolic function.

Anesthetics, Inhalation↗
PubMed1996

The susceptible patient.

Acute hypotension is a common complication of haemodialysis, occurring in 20-33% of patients in different series. Although the immediate cause is increasing intravascular hypovolaemia related to the dialysis procedure, no constant relationship exists between volume status or degree of volume loss and development of hypotension, emphasizing the importance of additional factors which render certain patients susceptible to this complication. These may include autonomic neuropathy, left ventricular hypertrophy (LVH) and diastolic dysfunction, inappropriate activation of cardiovascular reflexes, and abnormal vascular compliance. In contrast to earlier studies implicating autonomic neuropathy in intradialytic hypotension, recent reports have failed to confirm differences in autonomic function or baroreflex sensitivity in patients with and without hypotensive episodes. However, there is a strong association between LVH and dialysis hypotension. LVH is very common in ESRD, increases with time on dialysis, and is present in up to two-thirds of chronic dialysis patients. A close relationship exists between LVH and impaired diastolic relaxation, which is also common in ESRD patients. Patients prone to hypotension are characterized by both LVH and diastolic dysfunction, with an impaired early to late ventricular filling ratio, together with virtual complete cessation of passive ventricular filling prior to development of hypotension. Impaired cardiac filling and reduced cardiac output do not fully explain dialysis hypotension; in most subjects the response is reflex sympathetic activation and peripheral vasoconstriction, with maintenance of blood pressure. Syncope may result from activation of ventricular mechanoreceptor afferents as a response to left ventricular underfilling, with a resulting paradoxical withdrawal of sympathetic activity and of reflex vasoconstriction. Other potential factors increasing susceptibility to hypotension include impaired venous compliance, which predisposes to reduced venous return, seen particularly in elderly hypertensive and diabetic ESRD patients. Anaemia, inadequate vascular refilling rate, and overactivity of the NO vasodilator pathway have also been proposed to contribute to the pathogenesis of intradialytic hypotension. Excessive interdialytic weight gain is not directly related to hypotension, but EDTA data have shown it to be associated with increased cardiovascular mortality. Despite this, interdialytic weight gain is not related either to interdialytic blood pressure change, nor to development of LVH.

Blood Vessels↗
PubMed2005

Elevated NT-ProBNP levels in patients with increased left ventricular filling pressure during exercise despite preserved systolic function.

BACKGROUND: The role of brain natriuretic peptides in the detection of mild forms of isolated diastolic dysfunction is still uncertain. We therefore investigated the plasma levels of the N-terminal pro-B-type natriuretic peptide (NT-proBNP) in patients with heart failure symptoms during exercise, despite preserved systolic cardiac function. METHODS AND RESULTS: Fifteen control subjects and 15 symptomatic patients with preserved left ventricular ejection fraction of > or =50%, near normal Doppler echocardiographic indices, and left and right heart catheter indices at rest but increased filling pressures during exercise were studied. Plasma NT-proBNP levels and surrogate parameters of diastolic function were determined simultaneously. The median NT-proBNP plasma level was elevated (median, 145.2 pg/mL [range, 69.7-273.4 pg/mL] vs 38.3 pg/mL [range, 22.1-64.7 pg/ml]; P < .0001) in patients with increased filling pressure during exercise and correlated strongly with the pulmonary capillary wedge pressure (r = 0.78; P < .001). CONCLUSION: NT-proBNP levels are increased in patients with increased filling pressures during exercise and useful for the detection of diastolic dysfunction in patients with exertional dyspnea.

Adult↗
PubMed2001

Cardiac manifestations in Fabry disease.

Fabry disease is an X-linked recessive genetic disorder of glycosphingolipid metabolism, due to deficiency of the lysosomal enzyme alpha-galactosidase A. The disease is characterized by the progressive intracellular lysosomal accumulation of neutral glycosphingolipids throughout the body, including the cardiovascular system. It has been reported that cardiac involvement could be the sole manifestation of the disease in some patients. Myocardial abnormalities are characterized mainly by left ventricular (LV) wall thickening without significant cavity dilatation, the most frequent abnormal structural pattern being concentric LV hypertrophy (LVH). In some patients the disease mimics a typical hypertrophic obstructive cardiomyopathy. According to our experience, systolic function is largely preserved in a large majority of affected individuals. In contrast, mild to moderate impairment of diastolic filling is a relatively common finding, representing probably the most important cause of dyspnoea in patients with Fabry disease. However, in a relatively large population of affected patients, severe diastolic dysfunction, typical of restrictive cardiomyopathy, was not found. Valvular structural abnormalities are frequent due to valvular infiltration. In several patients, hypertrophy of papillary muscles and/or systolic anterior motion of the mitral leaflets associated with LV outflow obstruction may aggravate the mitral valve dysfunction. We did not confirm the previously reported high prevalence of mitral valve prolapse. Valvular regurgitation seems to be relatively frequent but mostly non-significant. Electrocardiographic changes in Fabry disease are multiple and include atrioventricular (AV) conduction abnormalities (abbreviation of the P-R interval or AV blocks), signs of LVH and repolarization abnormalities. Our observations suggest that conduction defects and repolarization changes are present predominantly in subjects with LV structural abnormalities. Cardiac symptoms in patients with Fabry disease include shortness of breath on effort (related to LV diastolic dysfunction), vasospastic and/or exertional angina pectoris (due to LVH, endothelial dysfunction and/or fixed coronary artery stenosis) and syncope (related to AV blocks or LV outflow obstruction). The extent of cardiac involvement, in particular LV mass assessment, could represent an ideal surrogate endpoint for evaluating the efficacy of specific therapies.

Electrocardiography↗
PubMed2005

Echocardiographic alterations in systemic sclerosis: a longitudinal study.

OBJECTIVE: To investigate the evolution of cardiac alterations in systemic sclerosis (SSc). METHODS: Echocardiographic and echo-Doppler findings from 77 unselected SSc patients were analyzed at the first clinical observation and after a follow-up period of 65 +/- 36 months. Data were compared with those obtained from 45 normal subjects matched for age and sex. RESULTS: Baseline left ventricular (LV) systolic function was normal in all patients and controls while LV diastolic dysfunction (expressed by an inverted E/A ratio which represents early and late filling of the LV during atrial contraction) was present in 23 patients and in 1 control ( P < 0.001). At the end of the follow-up period, while LV systolic function declined in 1 case alone, 6 further patients developed an inverted E/A ratio. Moreover, in the group of SSc patients mean A-wave values, E/A ratio, left atrial dimension, and LV wall thickness significantly changed, all indicating the progression of heart involvement. The alteration of LV diastolic function was independent of other known causes potentially affecting LV relaxation. Moreover, impairment of LV filling parameters was detected in the first phase of follow-up, while the anatomical changes occurred in the last phase. CONCLUSIONS: Our data confirm the significant prevalence of LV diastolic dysfunction in SSc patients and the role of primary myocardial involvement. The long-term follow-up demonstrates that LV filling dysfunction is progressive and precedes the occurrence of LV remodeling.

Adult↗
PubMed2003

Cross-linking of glycated collagen in the pathogenesis of arterial and myocardial stiffening of aging and diabetes.

The normal aging process is often accompanied by arterial wall stiffening and by a decrease in myocardial compliance. These processes contribute to isolated systolic hypertension and diastolic heart failure, which lead to substantial morbidity and mortality among older individuals. Patients with diabetes manifest arterial stiffening and diastolic dysfunction at a younger age. This leads to the concept that the mechanism that underlies changes in vascular mechanical properties during aging is accelerated in diabetes. The Maillard reaction or advanced glycation of proteins occurs slowly in vivo with normal aging and at an accelerated rate in diabetes. Advanced glycation end-products (AGEs) that form during the Maillard reaction are implicated in the complications of aging and diabetes. The formation of AGEs on vascular wall and myocardial collagen causes cross-linking of collagen molecules to each other. This leads to the loss of collagen elasticity, and subsequently a reduction in arterial and myocardial compliance. Aminoguanidine, an inhibitor of AGE formation, is effective in slowing or preventing arterial stiffening and myocardial diastolic dysfunction in aging and diabetic animals. In aged and diabetic animals, agents that can chemically break pre-existing cross-linking of collagen molecules are capable of reverting indices of vascular and myocardial compliance to levels seen in younger or non-diabetic animals. These studies suggest that collagen cross-linking is a major mechanism that governs aging and diabetes-associated loss of vascular and cardiac compliance. The development of AGEs cross-link breakers may have important role for future therapy of isolated systolic hypertension and diastolic heart failure in these conditions.

Aging↗
PubMed2000

New insights in cardiac structural changes in patients with Fabry's disease.

BACKGROUND: Fabry's disease is an X-linked recessive genetic deficiency of the enzyme alpha-galactosidase leading to the pathologic intracellular deposition of neutral glycosphingolipids. Although cardiac involvement is frequent, there is controversy regarding the character of the associated left ventricular (LV) changes and the severity of valvular involvement. METHODS: Clinical evaluation (disease severity scaling, laboratory tests, and echocardiography) was performed in 13 hemizygous men (mean age 39 +/- 10 years) and 17 heterozygous women (mean age 35 +/- 19 years). RESULTS: LV hypertrophy (LVH) was frequent in subjects older than 30 years, more often in men (61%) than in women (18%, P <.001). The degree of LVH was independently associated with age and the logarithm of alpha-galactosidase activity (r(2) = 0.70, P <.001). The predominant LV geometric patterns were concentric LVH and remodeling, both present in 11 subjects (36%). Three patients had an asymmetric septal hypertrophy mimicking hypertrophic cardiomyopathy. In most subjects with LVH, the systolic function was normal and severe diastolic dysfunction (restrictive pattern) was not noted. Minor structural abnormalities of the mitral valve were found in 17 subjects (57%). The aortic valve was affected in 14 patients (47%). Valvular abnormalities were frequently accompanied by regurgitation of minor to mild degree. The presence of LVH or valvular changes was associated with increased disease severity. CONCLUSIONS: Echocardiographically detectable cardiac involvement is frequent with Fabry's disease, particularly in older subjects, and more pronounced in affected hemizygous men than in heterozygous women. LVH is frequently observed but usually not associated with significant systolic or restrictive diastolic dysfunction. Concentric LVH and remodeling appear to be the major manifestations of LV structural alteration. The frequently noted valvular abnormalities were not associated with a significant degree of regurgitation. Valvular and especially LV structural changes may serve as a useful marker of disease severity.

Adolescent↗
PubMed1998

Constitutive properties of adult mammalian cardiac muscle cells.

BACKGROUND: The purpose of this study was to determine whether changes in the constitutive properties of the cardiac muscle cell play a causative role in the development of diastolic dysfunction. METHODS AND RESULTS: Cardiocytes from normal and pressure-hypertrophied cats were embedded in an agarose gel, placed on a stretching device, and subjected to a change in stress (sigma), and resultant changes in cell strain (epsilon) were measured. These measurements were used to examine the passive elastic spring, viscous damping, and myofilament activation. The passive elastic spring was assessed in protocol A by increasing the sigma on the agarose gel at a constant rate to define the cardiocyte sigma-versus-epsilon relationship. Viscous damping was assessed in protocol B from the loop area between the cardiocyte sigma-versus-epsilon relationship during an increase and then a decrease in sigma. In both protocols, myofilament activation was minimized by a reduction in [Ca2+]i. Myofilament activation effects were assessed in protocol C by defining cardiocyte sigma versus epsilon during an increase in sigma with physiological [Ca2+]i. In protocol A, the cardiocyte sigma-versus-epsilon relationship was similar in normal and hypertrophied cells. In protocol B, the loop area was greater in hypertrophied than normal cardiocytes. In protocol C, the sigma-versus-epsilon relation in hypertrophied cardiocytes was shifted to the left compared with normal cells. CONCLUSIONS: Changes in viscous damping and myofilament activation in combination may cause pressure-hypertrophied cardiocytes to resist changes in shape during diastole and contribute to diastolic dysfunction.

Actin Cytoskeleton↗
PubMed2004

[Factors influencing cardiac complications in patients with type-2 diabetes mellitus and silent myocardial ischaemia: five-year follow-up].

UNLABELLED: Silent myocardial ischaemia (SMI), a common disorder, has been studied by different research groups for the last 25 years. It is known that SMI is more common in patients with type 2 diabetes mellitus (type 2 DM) than in the general population, even though pathological mechanisms responsible for SMI are unclear. The aim of the study was to assess the role of SMI and other conditions in predicting adverse outcome in patients with type 2 DM during five years of follow-up. MATERIALS AND METHODS: 67 males with type 2 DM were enrolled into the study group. 55-healthy men were used as a control group (CG). Precise clinical examinations (medical history, physical examination, laboratory tests) were conducted. Coronary risk factors and the level of diabetes control were assessed. Noninvasive cardiological tests: ETT, 24 h ECG and echocardiography were performed. The prevalence of the following complications: ischaemia, unstable angina, myocardial infarction, heart failure, death and need for invasive procedures was recorded for five years. Parameters responsible for the complications were analyzed with the use of univariate logistic regression test; odds ratio was calculated. RESULTS: The silent myocardial ischaemia was found in 32.8% of patients with type 2 DM and in 9.1% men in control group (p < 0.001). The complications were observed in 24% of men with DM and in 16% in control group (NS). It was found that 25 parameters in the studied group and 16 parameters in the control group were statistically significant for the prediction of complications (among analyzed 92 parameters). The most important of them in type 2 DM group are: duration of diabetes (years) OR--1.18 (p < 0.01), fasting glucose (mg/dl) OR--1.017 (p < 0.01), SMI episodes (ETT) OR--4.72 (p < 0.01), diastolic dysfunction (E/A), OR--0.003 (p < 0.02) and left ventricle hypertrophy OR--3.86 (p < 0.05), whereas in CG--SMI episodes, OR--17.72 (p < 0.002). CONCLUSIONS: (1) The silent myocardial ischaemia is common in patients with type 2 DM. It was diagnosed in 33% of the patients. (2) The presence of SMI significantly increases the risk of complications both in patients with diabetes mellitus and the control group. (3) There are many other factors predisposing to the complications. In patients with diabetes mellitus they included, besides SMI, the duration of diabetes, chronic hyperglycemia and left ventricular diastolic dysfunction.

Adult↗
PubMedDate not supplied

[The use of delta-receptor antagonist DuP 734 for correction of the contractile diastolic cardiac dysfunction in reperfusion injury and oxidative stress].

Intraperitoneal administration of the sigma-receptor antagonist DuP 734 (1 mg/kg) 15 min before heart excision produces a decrease in the reperfusion heart contractility and prevented from the reperfusion induced cardiac cell lesion upon global ischemia of the isolated perfused rat heart. At the same time, a preliminary treatment with DuP 734 potentiated the reperfusion induced suppression of the cardiac pump function, while affecting neither the cardiac contractility dysfunction nor the cardiac cell injury during the oxidative stress. It is concluded that DuP 734 is not effective in preventing the myocardial stunning. The cardio-protector effect of DuP 734 during reperfusion is not related to inhibition of the free radical cell damage.

Anti-Arrhythmia Agents↗