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PubMed1993

From Left Ventricular Dysfunction to Heart Failure in the Elderly Patient.

The pathophysiology of the syndrome of congestive heart failure (CHF) is different in elderly patients compared to middle-aged subjects. When the syndrome of CHF predominantly results from left ventricular (LV) systolic dysfunction, peripheral mechanisms in elderly patients are less apt to compensate for the decline in LV performance due to deconditioning of the skeletal muscles, decreased vasodilatory response to exercise, and reduced capacity to excrete sodium. These all develop with age. LV diastolic dysfunction, i.e., LV filling impairment, appears to be a more frequent cause of CHF in elderly patients than in middle-aged subjects. Hypertrophy of the cardiac myocyte is associated with a prolongation of the calcium transient which, in turn, results from a decreased concentration of the enzyme responsible for reuptake of calcium in the sarcoplasmic reticulum. Cardiac myocyte hypertrophy results from a steady loss of myocytes and a progressive rise in arterial impedance which are both observed with aging. Notwithstanding subendocardial myocardial ischemia which is frequently associated with LV wall hypertrophy, prolongation of the calcium transient leads to impaired LV wall relaxation and the syndrome of LV diastolic dysfunction. The goals of therapy are also different in elderly patients compared to middle-aged patients. In elderly patients, one is less concerned about restoring a near normal exercise capacity, and aims at preventing acute episodes of decompensation which frequently accompany excessive sodium intake. Therefore, strict adherence to diet and careful titration of the dosages of medication to renal function are important considerations when treating CHF in elderly patients. In particular, cardiac glycosides, which should be avoided with CHF due to LV diastolic dysfunction, should be carefully titrated to creatinine clearance and body weight when treating elderly patients with LV systolic dysfunction in sinus rhythm. Similarly, the dosages of most angiotensin-converting enzyme inhibitors should be reduced in elderly patients.

Journal Article↗
PubMed2001

Early signs of cardiac involvement in hypertension.

BACKGROUND: Whether abnormalities of diastolic function are the earliest cardiac change in hypertension is still a matter for dispute. The aim of this study was to assess whether left ventricular diastolic dysfunction is an early sign of cardiac involvement in hypertension. METHODS: In 578 young patients with stage I hypertension from the Hypertension and Ambulatory Recording Venetia Study (HARVEST) and 101 normotensive control patients echocardiographic Doppler examination and ambulatory blood pressure monitoring were performed. RESULTS: Left ventricular mass, wall thickness, and relative wall thickness, adjusted for confounders, were greater in the hypertensive than in the normotensive patients (all P <.0001). After adjustment for confounders, the A-wave peak velocity was higher in the hypertensive patients (51.5 +/- 11.5 vs 43.4 +/- 8 cm/s, P <.001) as were A-wave velocity time integral (5.6 +/- 1.7 vs 4.6 +/- 1.3 cm, P =.01), total area (16.9 +/- 4.4 vs 15.6 +/- 3.1 cm, P =.04), and E-wave peak velocity (69.9 +/- 15.2 vs 67.5 +/- 13.3 cm/s, P =.03). All indexes of diastolic function were similar in the hypertensive subjects subdivided according to whether they had "white-coat" or sustained hypertension. Among the hypertensive subjects, age and heart rate were the strongest predictors of diastolic indexes, whereas ambulatory blood pressure explained only a marginal part of the E/A ratio, A-wave peak velocity, and the first one third total area ratio (P =.04, P =.02, and P =.05, respectively). Left ventricular mass and wall thickness were not associated with any Doppler index. When a clustering of diastolic indexes (E/A wave ratio, deceleration time, first one third of diastole, and peak E-wave-velocity) was used to identify subjects with diastolic dysfunction, no significant differences in either clinic or ambulatory blood pressure were observed between the group with diastolic dysfunction and the group with normal function. CONCLUSIONS: We conclude that the earliest signs of cardiac involvement in hypertension are left ventricular structural abnormalities. Left ventricular diastolic function is only marginally affected, even when multiple parameters of left ventricular filling are taken into account.

Adult↗
PubMed2004

Beta-blocker improves survival, left ventricular function, and myocardial remodeling in hypertensive rats with diastolic heart failure.

BACKGROUND: Chronic beta-blocker therapy improves survival and left ventricular (LV) systolic function in patients with congestive heart failure. However, its efficacy in diastolic heart failure (DHF) with preserved normal LV systolic function remains uncertain. METHODS: Dahl salt-sensitive hypertensive rats fed a high-salt diet from 7 weeks of age were randomized to groups that were either not treated (DHF; n = 20) or treated with metoprolol (MP) from 7 weeks of age (DHF+7wkMP; n = 22) or from 17 weeks of age (DHF+17wkMP; n = 8). Both LV function and remodeling were evaluated by serial echocardiography, followed by hemodynamic and pathologic studies. RESULTS: Hypertension and pressure-overload LV hypertrophy were established by 17 weeks of age in DHF rats. At about 20 weeks of age DHF rats experienced overt heart failure, which was accompanied not by a decrease in LV fractional shortening but by diastolic filling abnormalities. The LV concentric hypertrophy was strikingly attenuated in DHF+7wkMP rats but not in DHF+17wkMP rats. However, LV myocardial fibrosis and the further progression of diastolic dysfunction were prevented in both MP-treated groups. Survival at 21 weeks of age was significantly improved in DHF+7wkMP (86%) and DHF+17wkMP (75%) rats compared with DHF rats (25%). CONCLUSIONS: In this study, MP prevented not only the development of LV hypertrophy but also the progression of diastolic dysfunction, and improved survival in rats with DHF. The preventive effect of MP on myocardial fibrosis is suggested as one of the mechanisms contributing to halt the progression of diastolic dysfunction, a finding that may lead to clinical benefits in regard to DHF caused by hypertension.

Adrenergic beta-Antagonists↗
PubMed2002

Cardiac diastolic function and hypercapnic ventilatory responses in central sleep apnoea.

Hyperventilation is the key factor contributing to the development of idiopathic nonhypercapnic central sleep apnoea (ICSA), where left ventricular systolic function is normal. ICSA is reported to occur in 20% of patients with left ventricular diastolic dysfunction, in whom elevated pulmonary vascular pressures and resultant increased pulmonary vagal afferent traffic may contribute to hyperventilation. The contribution of the two potential mechanisms responsible for the hyperventilation seen in the following ICSA was measured: 1) left ventricular diastolic dysfunction-induced pulmonary hypertension; and 2) increased peripheral and central hypercapnic ventilatory responses (HCVR). The pulmonary artery pressure, left ventricular diastolic function and chemosensitivity to hypercapnia were measured during wakefulness in 16 subjects with ICSA. All subjects had systolic pulmonary artery pressures <3.99 kPa (<30 mmHg) and only four had diastolic dysfunction. All subjects had elevated peripheral and central HCVR compared with historical normal control subjects. Diastolic dysfunction correlated with increasing age but not with HCVR or markers of central sleep apnoea severity. Idiopathic nonhypercapnic central sleep apnoea is likely to be dependent upon raised hypercapnic ventilatory responses, and not pulmonary hypertension due to left ventricular diastolic dysfunction.

Adolescent↗
PubMed2006

Acute changes in left ventricular diastolic function: cigarette smoking versus nicotine gum.

BACKGROUND: Echocardiographic evidence of diastolic dysfunction has been demonstrated during acute cigarette smoking in patients with coronary artery disease. Similar studies in healthy patients have shown conflicting results. Furthermore, it is unclear whether nicotine or some other cigarette-related substance is responsible for these observations. HYPOTHESIS: The purpose of the study was to confirm or refute acute effects of cigarette smoking on diastolic function in healthy patients and to compare diastolic effects of a cigarette to smokeless nicotine delivery (nicotine gum). METHODS: In all, 27 healthy volunteers were self-assigned into one of two cohorts. A baseline echocardiogram was performed in all patients. The first cohort proceeded to smoke a cigarette and the second to chew a piece of nicotine gum. Within minutes after exposure, another echocardiogram was performed. Traditional measures of diastolic function were compared before and after substance exposure by paired t-tests. RESULTS: The cigarette cohort showed echocardiographic evidence of diastolic dysfunction after smoking. The E:A ratio (time integral) decreased from 2.95 to 2.22 (p < 0.002). Atrial reversal pulmonary velocity, atrial reversal duration, and color flow propagation all showed statistically significant alterations (p < 0.05). The nicotine gum cohort showed no change in traditional diastolic parameters. CONCLUSIONS: Diastolic function is impaired during acute exposure to cigarette smoke but unchanged after exposure to nicotine gum. It is therefore unlikely that nicotine alone is responsible for cigarette-induced acute diastolic dysfunction.

Adult↗
PubMed2004

Aging increases stiffness of cardiac myocytes measured by atomic force microscopy nanoindentation.

It is well established that the aging heart exhibits left ventricular (LV) diastolic dysfunction and changes in mechanical properties, which are thought to be due to alterations in the extracellular matrix. We tested the hypothesis that the mechanical properties of cardiac myocytes significantly change with aging, which could contribute to the global changes in LV diastolic dysfunction. We used atomic force microscopy (AFM), which determines cellular mechanical property changes at nanoscale resolution in myocytes, from young (4 mo) and old (30 mo) male Fischer 344 x Brown Norway F1 hybrid rats. A measure of stiffness, i.e., apparent elastic modulus, was determined by analyzing the relationship between AFM indentation force and depth with the classical infinitesimal strain theory and by modeling the AFM probe as a blunted conical indenter. This is the first study to demonstrate a significant increase (P < 0.01) in the apparent elastic modulus of single, aging cardiac myocytes (from 35.1 +/- 0.7, n = 53, to 42.5 +/- 1.0 kPa, n = 58), supporting the novel concept that the mechanism mediating LV diastolic dysfunction in aging hearts resides, in part, at the level of the myocyte.

Animals↗
PubMed2000

Infiltrative nonamyloidotic monoclonal immunoglobulin light chain cardiomyopathy: an underappreciated manifestation of plasma cell dyscrasias.

BACKGROUND: Infiltrative cardiomyopathies are characterized by diastolic dysfunction. In monoclonal plasma cell dyscrasias, organ compromise may be produced by tissue deposition of monoclonal immunoglobulins or their constituent peptides independently of the effects of unbridled plasma cell proliferation. The deposits may be fibrillar, as in light chain amyloid (AL) or nonfibrillar, as in light chain deposition disease (LCDD). AL disease of the heart is a restrictive cardiomyopathy. We hypothesized that, despite differences in physical properties, nonamyloidotic light chain deposition in the myocardium could produce similar clinical and physiological abnormalities. METHODS: Cardiac tissue from five patients with LCDD and cardiac dysfunction was examined by immunohistochemical and electron microscopic techniques. Hospital charts, electrocardiograms, echocardiograms and cardiac catheterization results were reviewed. In two cases, the original echocardiograms were reanalyzed. RESULTS: The five patients with nonamyloidotic light chain deposits in the myocardium had either mechanical or electrocardiographic abnormalities. In four with adequate clinical documentation, the diastolic dysfunction and conduction abnormalities were similar or identical to that described in cardiac AL disease. CONCLUSIONS: Although nonamyloidotic immunoglobulin light chain deposits in the myocardium differ in distribution and ultrastructural organization from the fibrillar deposits of AL disease, an analogous pattern of diastolic dysfunction and conduction disturbances results. The diagnosis should be considered in patients with a plasmacytic dyscrasia and restrictive cardiomyopathy in whom Congo red staining of endomyocardial biopsy tissue is negative. The diagnosis can be established by using the appropriate immunohistochemical and ultrastructural tissue examinations.

Adult↗
PubMed2004

Utility of B-natriuretic peptide in the evaluation of left ventricular diastolic function: comparison with tissue Doppler imaging recordings.

BACKGROUND: Although Doppler echocardiography provides assessment of abnormal left ventricular (LV) diastolic filling dynamics, its inherent limitations suggest the need for additional measures of diastolic dysfunction. The ratio of mitral velocity to early diastolic velocity of the mitral annulus (E/E') derived from tissue Doppler imaging is associated with the mean LV end diastolic pressure (LVEDP). Because data suggest that B-natriuretic peptide (BNP) reflects ventricular pressure, we hypothesized that BNP levels correlate with indices of LV diastolic function by tissue Doppler imaging. METHODS AND RESULTS: Doppler recordings of the mitral inflow and tissue Doppler imaging of the mitral annulus were obtained in 108 patients referred for echocardiography. BNP levels were measured by a rapid immunoassay and blinded to cardiologists making the assessment of LV function. BNP levels were higher when elevated E/E' ratios derived from tissue Doppler imaging were identified. Patients identified with elevated LVEDP, defined as E/E' >15 (n = 16), had the highest BNP levels (463 +/- 80 pg/mL). Those with normal LVEDP, as predicted by E/E' <8 (n = 36), had a mean BNP concentration of 97 +/- 27 pg/mL. Those with E/E' of 8 to 15 (n = 48) had a mean BNP level of 122 +/- 24 pg/mL. The area under the receiver-operating curve for BNP to detect E/E' >15 was 0.89 (95% CI, 0.82 to 0.96; P < .001). A BNP value of 173 pg/mL had a sensitivity of 88%, a specificity of 82%, and an accuracy of 83% for predicting E/E' >15. CONCLUSIONS: BNP levels correlate with the E/E' ratios from tissue Doppler imaging (r = 0.48) and can reliably provide estimation of LV filling pressures. Although BNP levels do not correlate well with E/E' ratios across the full spectrum of values, the combination of BNP levels along with E/E' ratios from tissue Doppler imaging may be a better predictor of elevated LV filling pressures in patients with suspected diastolic dysfunction.

Adult↗
PubMed2000

[Cardiac failure in ischemic cardiopathy].

Heart failure is a major cause of morbidity and mortality and represents an important recognized health problem. Heart (or cardiac) failure is the pathophysiological state in which a myocardial dysfunction is frequently but non always responsible for the inability of the heart to pump blood at a rate commensurate with tissues metabolic requirements. Ischemic heart disease is the commonest cause of heart failure frequently associated with left ventricular systolic dysfunction, although some patients, particularly the elderly, have diastolic dysfunction. Coronary heart disease is responsible for left ventricular systolic dysfunction (and cardiac failure) in the acute and chronic stage. Myocardial dysfunction is usually a consequence of myocardial infarction that may lead to ventricular remodeling with compensatory dilation and hypertrophy and subsequent systolic and diastolic dysfunction resulting in heart failure. Many patients with heart failure and/or left ventricular dysfunction are unknown. The echocardiographic screening of patients with known or suspected left ventricular dysfunction remains an important topic for future clinical epidemiological research and allows for improvement of therapeutic management of patients with cardiac dysfunction.

Echocardiography↗
PubMed2005

Plasma B-type natriuretic peptide levels are associated with early cardiac dysfunction after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Serum B-type natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), as well as in the setting of congestive heart failure and myocardial infarction. The aim of this study was to prospectively quantify the relationship between BNP levels and cardiac outcomes after SAH. METHODS: Plasma was collected for BNP measurements as soon as possible after enrollment; a mean of 5+/-4 days after SAH symptom onset. On days 1, 3, and 6 after enrollment, troponin I (cTi) was measured and 2-dimensional echocardiography was performed. The following cardiac variables were collected and treated dichotomously: left ventricular ejection fraction (LVEF), regional wall motion abnormalities (RWMA), diastolic dysfunction, pulmonary edema, and cTi. RESULTS: There were 57 subjects. The median BNP level was 141 pg/mL (range, 0.8 to 3330 pg/mL). Higher mean BNP levels were present in those with RWMA (550 versus 261 pg/mL; P=0.012), diastolic dysfunction (360 versus 44; P=0.011), pulmonary edema (719 versus 204; P=0.016), elevated cTi (662 versus 240; P=0.004), and LVEF <50% (644 versus 281; P=0.015). CONCLUSIONS: Early after SAH, elevated BNP levels are associated with myocardial necrosis, pulmonary edema, and both systolic and diastolic dysfunction of the left ventricle. These findings support the hypothesis that the heart releases BNP into the systemic circulation early after SAH.

Aged↗
PubMed1990

[Heart effect of arterial hypertension. Heart hypertrophy as a risk factor. Study technics (electrocardiogram, echocardiography, exercise test and Holter].

Left ventricular hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. There are multiple mechanisms in which left ventricular hypertrophy may account for this excess mortality including increased incidence of arrhythmias, systolic an diastolic dysfunction, relative ischemia, and associated coronary artery disease. Diastolic dysfunction, manifested by reduced ventricular distensibility of the hypertrophic 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 left ventricular hypertrophy appears. The presence of left ventricular hypertrophy is difficult to detect by electrocardiography. Echocardiography seems to be the best non-invasive method for the detection of hypertensive heart disease: it shows early abnormalities of left ventricular compliance, frequently left ventricular hypertrophy and late abnormalities of myocardial contractility.

Arrhythmias, Cardiac↗
PubMed2002

Echocardiographic assessment of cardiac function in diabetic db/db and transgenic db/db-hGLUT4 mice.

Control db/+ and diabetic db/db mice at 6 and 12 wk of age were subjected to echocardiography to determine whether contractile function was reduced in vivo and restored in transgenic db/db-human glucose transporter 4 (hGLUT4) mice (12 wk old) in which cardiac metabolism has been normalized. Systolic function was unchanged in 6-wk-old db/db mice, but fractional shortening and velocity of circumferential fiber shortening were reduced in 12-wk-old db/db mice (43.8 +/- 2.1% and 8.3 +/- 0.5 circs/s, respectively) relative to db/+ control mice (59.5 +/- 2.3% and 11.8 +/- 0.4 circs/s, respectively). Doppler flow measurements were unchanged in 6-wk-old db/db mice. The ratio of E and A transmitral flows was reduced from 3.56 +/- 0.29 in db/+ mice to 2.40 +/- 0.20 in 12-wk-old db/db mice, indicating diastolic dysfunction. Thus a diabetic cardiomyopathy with systolic and diastolic dysfunction was evident in 12-wk-old diabetic db/db mice. Cardiac function was normalized in transgenic db/db-hGLUT4 mice, indicating that altered cardiac metabolism can produce contractile dysfunction in diabetic db/db hearts.

Animals↗
PubMed2004

Tissue inhibitor of metalloproteinase-1 and matrix metalloproteinase-9 levels in patients with hypertension Relationship to tissue Doppler indices of diastolic relaxation.

BACKGROUND: Hypertension, hypertensive heart disease, and left ventricular (LV) hypertrophy are integral to symptomatic diastolic heart failure. Tissue inhibitor of metalloproteinase-1 (TIMP-1) is linked to extracellular matrix fibrosis and is elevated in hypertension. We hypothesized a link between circulating TIMP-1, matrix metalloproteinase-9 (MMP-9), and resting echocardiographic LV filling parameters using tissue Doppler parameters of diastolic (dys)function. METHODS: Circulating MMP-9 and TIMP-1 levels were measured in citrated plasma by ELISA in 74 patients with hypertension (58 men, mean age 58 +/- 11 years) and 34 controls (23 men, mean age 53 +/- 13 years). All had confirmed normal short axis systolic contractility, with no significant wall motion abnormalities; the LV mass and standard resting tissue Doppler echocardiographic indices of diastolic function were also recorded. RESULTS: Both MMP-9 and TIMP-1 levels were higher in the hypertensive group (P =.0039 and P =.0054, respectively). When compared to controls, hypertensive patients had a greater LV mass (P =.0054), and differences in many of the parameters reflecting diastolic dysfunction (controls versus hypertensives: E: 0.71 +/- 0.15 v 0.81 +/- 0.15 m/sec, P =.004; A: 0.66 +/- 0.12 v 0.81 +/- 0.16 m/sec, P <.0001; e': 0.12 (0.09-0.14) v 0.09 (0.07-0.10) m/sec, P =.0017; e'/a': 1.20 (1.00-1.80) v 0.88 (0.71-1.05), P <.0001; E/e': 6.54 (4.75-7.14) v 8.89 (7.55-10.75), P <.0001, respectively). Within the hypertensive cohort, only TIMP-1 levels correlated with LV mass (r = 0.271, P =.024), LV mass index (r = 0.323, P =.007), and tissue Doppler parameters of diastolic dysfunction, including e' (r = -0.338, P =.005), a' (r = -0.350, P =.005), and E/e' (r = 0.334, P =.005). CONCLUSIONS: TIMP-1 is thought to increase tissue concentrations of collagen type I by preventing its breakdown by MMPs. Our findings therefore add weight to a hypothesis suggesting that TIMP-1 may be a key mediator of LV diastolic dysfunction through definition of ventricular matrix composition.

Adult↗
PubMed2003

Diastolic function assessment incorporating new techniques in Doppler echocardiography.

Congestive heart failure (CHF) is the leading cause of cardiac morbidity and mortality from cardiovascular disease. Although left ventricular (LV) diastolic dysfunction occurs in all patients with systolic dysfunction and CHF, fully one third of patients have CHF due to isolated diastolic dysfunction. Despite this, the role of diastolic function in heart failure is underappreciated by many primary care physicians and even by cardiologists. Development and validation of several noninvasive Doppler echocardiographic techniques that are relatively load-independent have made echocardiography the clinical standard for the assessment of LV diastolic function. Echocardiography uses portable equipment; is readily accessible and safe; and excludes other causes of CHF, such as valvular heart disease, pericardial disease, and systolic dysfunction. This review summarizes the use of recently developed Doppler techniques for the assessment of LV diastolic function, as well as their application in assessing prognosis and in guiding therapy for various cardiovascular disease states.

Aged↗
PubMed1997

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly.

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.

Aged↗
PubMed2004

Diastolic heart failure: the forgotten manifestation of hypertensive heart disease.

Heart failure (HF) is a progressively debilitating disorder characterized by frequent hospital admissions and high annual mortality rates. Coronary artery disease (CAD), hypertension, and aging are major risk factors for the development/progression of HF. For years, most of the attention has been focused on HF caused by reduced left ventricular (LV) systolic function, largely attributable to CAD. It is now generally accepted that nearly 50% of elderly patients with HF might have normal or preserved LV systolic function. This condition is commonly referred to as a distinct type of HF caused by LV diastolic dysfunction, and it often accompanies hypertensive heart disease. Isolated diastolic HF is increasingly recognized as the dominant cause of symptoms and hospitalizations from HF in a large proportion of individuals aged 65 and older. However, the clinicians caring for patients with diastolic HF do not fully understand its cause, how it progresses, or how it could be appropriately diagnosed and treated. Because varying degrees of systolic and diastolic dysfunction might coexist in any individual patient, and given the limitation of current diagnostic tools, the overall impact of isolated diastolic HF continues to evolve. Ongoing clinical trials are testing new strategies for treatment of diastolic HF.

Coronary Artery Disease↗
PubMed1999

[Left ventricular diastolic function evaluated by Doppler echocardiography in coronary artery disease in relation to to systolic function].

The aim of the study was to assess the relationship between left ventricular (LV) diastolic dysfunction measured by Doppler mitral flow indices (D.m.f.i.) and LV systolic performance in coronary artery disease (CAD). 107 pts with confirmed CAD without or after MI in I, II NYHA class was divided into 2 groups according to ejection fraction (EF) value = 55%. 13 D.m.f.i. regarding to the time, velocity, flow volume and derivates were calculated. In the patient with CAD with normal EF, the diastolic dysfunction was characterised by the impaired relaxation. There were prolonged isovolumic relaxation time IVRT and deceleration time of early filling flow DT, reduced early filling fraction EFF and increased the atrial filling fraction AFF, decreased E/A ratio and E/A-VTI. The regression analysis revealed the positive correlation between EF and DT r = 0.35 and inverse correlation between wall motion score index WMSI and DT r = DT r = -0.33. The stepwise regression analysis revealed that EF and WMSI are independent factors influencing on DT. Our results confirm that diastolic dysfunction precedes the systolic dysfunction in CAD. The correlation between D.m.f.i. and LV systolic function parameters were obtained. The results suggest that the LV systolic function should be take to account in the Doppler mitral flow analysis.

Adolescent↗
PubMed1996

Left ventricular diastolic function in hypertension and role of plasma glucose and insulin. Comparison with diabetic heart.

BACKGROUND: Experimental production of glucose intolerance has been associated with increased diastolic stiffness of the left ventricle, accompanied by interstitial fibrosis. Because carbohydrate metabolism is altered in hypertension, we undertook the present study to assess the relation of diastolic dysfunction in hypertension to plasma glucose and insulin concentrations. The latter are also affected by obesity. To facilitate this analysis, we studied moderately obese hypertensives. Elucidation of these relations was then sought in diabetic subjects. METHODS AND RESULTS: Subjects undergoing catheterization for chest pain were included in the study when significant coronary disease was not present. In groups 1 (lean), 2 (obese), 3 (lean hypertensive), and 4 (obese hypertensives), intraventricular pressures and volumes were determined. Fasting plasma glucose, insulin, hemoglobinAIC, and glucose tolerance were assessed. Basal ejection fraction and end-systolic wall stress were normal in the four groups. Chamber stiffness was significantly elevated in the hypertensives and was higher in group 4 than in group 3 (P < .05). Diastolic dysfunction was correlated with fasting blood glucose (r = .69, P < .006) but not with plasma insulin or left ventricular mass. Chamber stiffness was also increased in diabetics, with a larger effect in the obese. CONCLUSIONS: Hypertension is associated with increased diastolic stiffness of the left ventricle, which is enhanced by moderate obesity, and abnormal carbohydrate metabolism. Experimentally and in humans, hypertension is associated with interstitial fibrosis of mycardium, the presumed basis for the diastolic dysfunction. Chamber stiffness in group 4 hypertensives was similar to that in the lean diabetics but less than that in the obese diabetics. Although the latter exhibited a correlation with plasma hemoglobinAIC, the large rise in stiffness suggests a potential role for growth factors in further alteration of myocardial composition.

Blood Glucose↗