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PubMed2004

Left atrial myopathy in cardiac amyloidosis: implications of novel echocardiographic techniques.

AIMS: To assess left atrial (LA) function and determine the prevalence of LA dysfunction in AL amyloidosis (AL) using conventional and strain echocardiography. METHODS AND RESULTS: LA ejection fraction, LA filling fraction, LA ejection force, peak LA systolic strain rate (LAsSR), and LA systolic strain (LA epsilon) were determined in 95 AL patients (70 with and 25 without echocardiographic evidence of cardiac involvement, abbreviated CAL and NCAL, respectively), 30 age-matched controls (CON), and 20 patients with diastolic dysfunction and LA dilatation (DD). Peak LAsSR >2 standard deviations below mean CON value was used as the cut-off for normal LA function. LA ejection fraction was lower in CAL when compared with CON (40.4+/-13.6 vs. 67.0+/-6%, P=0.01). Left atrial septal strain rate and strain were lower in CAL (0.8+/-0.5 s(-1) and 5.5+/-4%, respectively) compared with CON (1.8+/-0.8 s(-1) and 14+/-4%, respectively, P=<0.0001), NCAL (1.6+/-0.8 s(-1) and 13+/-7%, respectively, P<0.0001) and DD (1.3+/-0.4 s(-1) and 10+/-2%, respectively, P<0.0001). Based on peak LA systolic strain rate criteria, the cut-off values for normal LA function were -1.1 s(-1) and -1.05 s(-1) for lateral and septal walls. Using these criteria, LA dysfunction was identified in 32% (lateral LA criteria) and 60% (septal LA criteria) of CAL patients. Lateral and septal LAsSR were lower in CAL patients with vs. those without symptoms of heart failure. Inter- and intra-observer agreement was high for LA strain echocardiography. CONCLUSION: LA function assessment using strain echocardiography is feasible with low intra- and inter-observer variability. LA dysfunction is observed in AL patients without other echocardiographic features of cardiac involvement and may contribute to cardiac symptoms in CAL.

Aged↗
PubMed2004

Early detection of sympathetic myocardial denervation in patients with familial amyloid polyneuropathy type I.

INTRODUCTION: Type I familial amyloid polyneuropathy (FAP I) is an autosomal dominant inherited disorder due to a genetic defect in transthyretin and is characterized by deposition of amyloid in various organs and tissues. The principal manifestations are related to polyneuropathy and dysautonomia. The aim of this study was to assess cardiac involvement and to correlate the findings with neurological status. METHODS: 34 patients with FAP (15 male and 19 female; mean age 43 +/- 15 years) underwent I123-labeled metaiodobenzylguanidine (MIBG) myocardial scintigraphy in order to evaluate cardiac sympathetic innervation. In addition they underwent ambulatory blood pressure monitoring (ABPM) and two-dimensional and Doppler echocardiography. Neurological involvement was quantified according to a neurophysiologic score (EMG; 0 = no abnormality and 100% = maximal disability). RESULTS: The mean value of cardiac MIBG uptake was 1.75 +/- 0.5 (normal = 2.6 +/- 0.3) and correlated inversely with the EMG score (r = -0.67; p = 0.001). In 27 (79%) of the 34 patients there was a decrease in MIBG accumulation, in 18 (53%) an alteration in the circadian BP pattern and/or an increase in systolic and/or diastolic BP loads at night, and in 17 (50%) left ventricular hypertrophy and/or diastolic dysfunction. Twenty-two patients were symptomatic and had a mean EMG score of 37.7 +/- 25% (group I). The remaining 12 were asymptomatic and without neurological involvement (group II). Group I was characterized by older age (48 +/- 15 vs. 33 +/- 10.2 years, p = 0.01), lower MIBG uptake (1.5 +/- 0.4 vs. 2.2 +/- 0.5, p = 0.001), higher systolic (129 +/- 16 vs. 119 +/- 6 mmHg, p = 0.01) and diastolic daytime BP (82 +/- 10 vs. 76 +/- 6 mmHg, p = 0.05), and higher systolic (119 +/- 17 vs. 105 +/- 7 mmHg, p = 0.01) and diastolic nocturnal BP (71 +/- 11 vs. 62 +/- 9 mmHg, p = 0.01) than patients in group II. In 21/22 patients in group I and in 6/12 in group II there was a decrease in cardiac MIBG activity. Sixteen patients in group I and 2 in group II had abnormal circadian BP pattern. Left ventricular hypertrophy was only seen in group I. CONCLUSIONS: Patients with FAP have a high incidence of cardiac denervation and an abnormal circadian BP pattern. These alterations in cardiac autonomic function precede the development of clinical manifestations and may be an important factor in determining the optimal timing for liver transplantation, which is currently the only way to control the progression of the disease.

Adult↗
PubMed2003

Assessment of left ventricular systolic and diastolic functions in children with merosin-positive congenital muscular dystrophy.

Cardiopathy is an expected finding in X-linked Duchenne and Becker muscular dystrophies. This holds true for some other forms such as autosomal recessive limb-girdle dystrophies. However, data on early-onset and usually severe congenital muscular dystrophies are limited. The purpose of this study was to investigate the presence of cardiac involvement in children with merosin-positive congenital muscular dystrophy. A total of 42 patients and 22 healthy subjects were evaluated by M-mode, 2D, and Doppler echocardiography. Cardiac anatomy, left ventricular dimensions, wall thickness and systolic and diastolic functions were investigated in patients and compared with those of healthy control subjects. Mean left ventricular ejection fraction and shortening fraction were significantly lower in the patient group (P<0.05 and P<0.001, respectively) and in three patients ejection fraction was below 55%. Although some impairments in left ventricular inflow indexes which were suggestive of left ventricular diastolic dysfunction were detected in patients with merosin-positive congenital muscular dystrophy they were not statistically significant. Our results suggest that left ventricular systolic abnormalities may occur in children with merosin-positive congenital muscular dystrophy.

Adolescent↗
PubMed2005

A noninvasive method for assessing impaired diastolic suction in patients with dilated cardiomyopathy.

BACKGROUND: Diastolic suction is a major determinant of early left ventricular filling in animal experiments. However, suction remains incompletely characterized in the clinical setting. METHODS AND RESULTS: First, we validated a method for measuring the spatio-temporal distributions of diastolic intraventricular pressure gradients and differences (DIVPDs) by digital processing color Doppler M-mode recordings. In 4 pigs, the error of peak DIVPD was 0.0+/-0.2 mm Hg (intraclass correlation coefficient, 0.95) compared with micromanometry. Forty patients with dilated cardiomyopathy (DCM) and 20 healthy volunteers were studied at baseline and during dobutamine infusion. A positive DIVPD (toward the apex) originated during isovolumic relaxation, reaching its peak shortly after mitral valve opening. Peak DIVPD was less than half in patients with DCM than in control subjects (1.2+/-0.6 versus 2.5+/-0.8 mm Hg, P<0.001). Dobutamine increased DIVPD in control subjects by 44% (P<0.001) but only by 23% in patients with DCM (P=NS). DIVPDs were the consequence of 2 opposite forces: a driving force caused by local acceleration, and a reversed (opposed to filling) convective force that lowered the total DIVPD by more than one third. In turn, local acceleration correlated with E-wave velocity and ejection fraction, whereas convective deceleration correlated with E-wave velocity and ventriculo:annular disproportion. Convective deceleration was highest among patients showing a restrictive filling pattern. CONCLUSIONS: Patients with DCM show an abnormally low diastolic suction and a blunted capacity to recruit suction with stress. By raising the ventriculo:annular disproportion, chamber remodeling proportionally increases convective deceleration and adversely affects left ventricular filling. These previously unreported mechanisms of diastolic dysfunction can be studied by using Doppler echocardiography.

Adult↗
PubMed1995

The use of the handgrip maneuver to identify left ventricular diastolic function abnormalities by Doppler echocardiography in patients with coronary artery disease.

Doppler echocardiography accurately identifies diastolic dysfunction through the assessment of transmitral flow patterns during the application of the handgrip (HG) maneuver. In this study, 45 normal control patients (mean age 46 +/- 9, group A) and 13 patients with coronary artery disease (CAD) (mean age 51 +/- 6, group B) were involved. The effects of handgrip maneuver on transmitral flow patterns were studied by Doppler echocardiography. Group B patients had higher peak late diastolic filling velocities (A), lower peak early (E) to late diastolic filling velocity ratios (E/A) and longer isovolumic relaxation times (IVRT) compared to group A. On the other hand, systolic blood pressure (SBP), heart rate (HR) and peak E velocity (E) did not change significantly (p > 0.05) in either group, at rest. During the supine handgrip maneuver, NR (mean +/- standard error of mean, +21 +/- 13%, p < 0.05) and SBP (+21 +/- 9%, p < 0.05) increased significantly in both group A and group B (+21 +/- 13%, p < 0.05, +22 +/- 15%, p < 0.05, respectively). In group B, E/A ratio (-28 +/- 7%) decreased significantly (p < 0.05) compared to group A (-20 +/- 6%), as a consequence of significantly increased peak A velocity in group B (+7 +/- 5%) compared to group A (+6 +/- 3%, p < 0.05). Deceleration time decreased significantly in both groups (-10 +/- 6% vs -9 +/- 6%, p < 0.05). Isovolumic relaxation time (IVRT) significantly increased in both groups (+18 +/- 7% vs +16 +/- 6%, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Cardiac angiotensin converting enzyme and diastolic function of the heart.

It has been known for a long time that systemic infusion of angiotensin II in patients with coronary artery disease or normal control subjects causes a marked increase in left ventricular end diastolic pressure (LVEDP) and systolic pressure (LVP) (1,2). In this setting angiotensin II produces a marked increase in afterload that makes it difficult to acknowledge possible local myocardial effects of the peptide. The studies (3-8) summarized in the present paper were designed to examine the physiological role of local cardiac angiotensin II generation and local bradykinin degradation on cardiac function in the normal and hypertrophied rat heart. Angiotensin I and angiotensin II, infused in isolated, well oxygenated, buffer perfused normal rat hearts, produced a mild increase in LVEDP with no change in systolic function (3). In contrast, in hypertrophied rat hearts, angiotensin I and angiotensin II caused a marked deterioration of diastolic function, increasing LVEDP from 10 to 25-37 mmHg on average (3,5). Preliminary evidence suggests that angiotensin II effects on diastolic function are mediated via a protein kinase C dependent pathway that might involve Na+/H+ exchange (4,5). When cardiac angiotensin converting enzyme was blocked by infusion of an ACE inhibitor prior and in parallel to angiotensin I infusion no changes in diastolic function were noted (6). Furthermore, ACE inhibition blunted the diastolic dysfunction during low flow ischemia in isolated hypertrophied rat hearts (7). This effect of ACE inhibition was even more remarkeable, since no exogenous angiotensin was infused in this experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1996

[Oral vasodilators in the treatment of congestive heart failure].

Oral vasodilators have proved to be valuable drugs in the management of systolic or diastolic congestive heart failure. They produce a clinical and hemodynamic relief of preload, afterload or both during the resting state or exercise. Although left ventricular hypertrophy is an adaptative response to myocardial stress, in the long run it becomes an independent risk factor leading to diastolic dysfunction. At present, pharmacological regression of ventricular hypertrophy has a prognostic importance. Of the large number of available vasodilators, angiotensin converting enzyme inhibitors have proved to be the most successful drugs. They behave as afterload relievers, counteracting both the renin-angiotensin and adrenergic systems, but also are powerful inhibitors of cardiomyocite enlargement and interstitial connective tissue proliferation. This last structural change may revert the compromised diastolic function of the heart.

Administration, Oral↗
PubMed1997

Cardiopulmonary effects of endothelin-1 in man.

OBJECTIVES: Endothelin-1 levels are elevated in a number of conditions characterised by impaired cardiovascular performance and abnormal vasoconstriction such as congestive cardiac failure and primary and secondary pulmonary hypertension. The aim of the present study was to assess the effects of the vasoconstrictor peptide endothelin-1 on pulmonary and systemic haemodynamics and cardiovascular performance in normal man. METHODS: Ten healthy male volunteers were studied on two occasions in a randomised, double-blind, placebo-controlled, cross-over study and received systemic infusions of either endothelin-1 (0.75, 1.5 and 3 pmol.kg-1.min-1 for 30 min each) or saline placebo. Systemic and pulmonary haemodynamic parameters were monitored non-invasively by pulsed-wave Doppler, as were parameters of left and right ventricular diastolic filling and inotropic state. Effects on renin-angiotensin and natriuretic peptide system activity were also measured. RESULTS: Endothelin-1 infusion produced dose-related falls in heart rate, stroke volume and cardiac output. Systemic vascular resistance (SVR) increased from 1156 +/- 57 to 1738 +/- 115 dyn.s.cm-5, and total pulmonary vascular resistance (TPR) increased from 142 +/- 12 to 329 +/- 22 dyn.s.cm-5. Endothelin-1 caused significant impairment of left and right ventricular diastolic filling, even at a low dose which had no pulmonary or systemic pressor effects. Electromechanical and Doppler acceleration indices of inotropic state were also significantly impaired. Activity of the renin-angiotensin system was suppressed by endothelin-1 whilst plasma levels of atrial natriuretic peptide (ANP) were unchanged. CONCLUSIONS: Thus, in addition to systemic and pulmonary pressor effects our results suggest that endothelin-1 impairs overall cardiovascular performance by causing diastolic dysfunction and acting as a negatively inotropic agent. These effects were associated with compensatory changes in the renin-angiotensin system.

Adult↗
PubMed1998

Synergistic exacerbation of diastolic stiffness from short-term tachycardia-induced cardiodepression and angiotensin II.

Synergistic interaction between angiotensin II (Ang II) and evolving cardiodepression may play an important role in worsening chamber function, particularly in diastole. To test this hypothesis, Ang II was infused at 10 or 17 ng.kg(-1).min(-1) in 18 conscious dogs 4 days before and during induction of subacute cardiodepression by 48-hour tachypacing. The lower dose yielded negligible systemic pressure changes. Twelve additional animals served as paced-only controls. Pressure-dimension relations were recorded, and serial endocardial biopsies were obtained to assess histological and metalloproteinase (MMP) changes. Forty-eight-hour pacing alone depressed systolic function but had little effect on diastolic stiffness. Ang II alone only modestly raised diastolic stiffness at both doses and enhanced contractility at the higher dose. These changes recovered toward baseline after a 7-day infusion. However, Ang II (at either dose) combined with 48-hour pacing markedly increased ventricular stiffness (110+/-26% over baseline) and end-diastolic pressure (22+/-1.7 mm Hg). In contrast, pacing-induced inotropic and relaxation abnormalities were not exacerbated by Ang II. Zymography revealed MMP activation (72- and 92-kD gelatinases and 52-kDa caseinase) after a 4-day Ang II infusion (at both doses), which persisted during pacing. Tachypacing initiated 24 hours after cessation of a 7-day Ang II infusion also resulted in diastolic stiffening and corresponded with MMP reactivation. Ang II also induced myocyte necrosis, inflammation, and subsequent interstitial fibrosis, but these changes correlated less with chamber mechanics. Thus, Ang II amplifies and accelerates diastolic dysfunction when combined with evolving cardiodepression. This phenomenon may also underlie Ang II influences in late-stage cardiomyopathy, when chamber distensibility declines.

Angiotensin I↗
PubMedDate not supplied

Ambulatory blood pressure monitoring: technique and application in the study of cardiac dysfunction and congestive heart failure.

Ambulatory blood pressure monitoring has become a widely used method of blood pressure and heart rate evaluation in the free-living subject. Recently, ambulatory monitoring has become covered by Medicare for the evaluation of "white-coat" hypertension. Although the technique provides only intermittent readings throughout the 24-hour period, average blood pressures obtained in this way correlate well with a variety of hypertensive disease processes and are also a better prognostic marker for future cardiovascular events than office blood pressure. Ambulatory blood pressure averages also correlate well with indices of diastolic dysfunction. In patients with congestive cardiac failure and systolic dysfunction, ambulatory monitoring suggests an impaired circadian blood pressure profile with high nocturnal blood pressure. Further research is needed on the relationship between ambulatory blood pressure and cardiac dysfunction, as well as the impact of observed circadian blood pressure changes on outcome. (c)2001 CHF, Inc.

Journal Article↗
PubMed1999

Cardiac and autonomic evaluation in a pediatric population with human immunodeficiency virus.

BACKGROUND: Cardiac involvement in children with human immunodeficiency virus (HIV) infection is a well-known entity and occurs clinically more often in patients with advanced acquired immunodeficiency syndrome (AIDS). Autonomic dysfunction is less known, especially in children. HYPOTHESIS: The aim of this study was to asses the prevalence of cardiovascular abnormalities in a pediatric population with HIV. We also aimed to evaluate whether autonomic involvement occurs in the same population and is dependent on echocardiographic abnormalities. METHODS: The occurrence of echocardiographic abnormalities was evaluated in 22 children with HIV infection, and five noninvasive tests were performed to evaluate the presence of autonomic dysfunction. RESULTS: We found cardiac lesions in four children (18%), consisting of pericardial effusion in three children, wall motion abnormalities in three children, and acute aortic endocarditis in one child. All cardiac abnormalities were found at Stage C by Center for Disease Control (CDC) revised classification. We also found left ventricular filling pattern abnormalities consisting of E-wave maximal velocity decrease and prolonged deceleration time compatible with diastolic dysfunction. One of the five autonomic tests (Valsalva maneuver) was significantly altered, even in patients without abnormal echocardiography, suggesting mild autonomic dysfunction. CONCLUSION: The study demonstrated a high prevalence of cardiac lesions in children with HIV infection and indicated the presence of autonomic dysfunction even when there are no echocardiographically detected abnormalities.

Adolescent↗
PubMed1995

Cardiac renin-angiotensin system: role in development of pressure-overload hypertrophy.

Recent studies are reviewed dealing with the putative roles of the cardiac renin-angiotensin system in the development of pressure-overload hypertrophy and the subsequent transition from adaptive hypertrophy to diastolic dysfunction, impaired systolic function and cardiac failure. The results of these studies, which employed the aortic banded rat model of cardiac hypertrophy, indicate that the intracardiac conversion of angiotensin I (Ang I) to angiotensin II (Ang II) is significantly increase in hypertrophied hearts compared with hearts from age-matched, sham-operated controls, and that Ang II may have a direct effect of slowing relaxation and altering diastolic tone in the hypertrophied heart. Furthermore, in patients with aortic stenosis and severe baseline abnormalities of diastolic relaxation and filling, acute intracardiac angiotensin-converting enzyme (ACE) inhibition, totally in the absence of any systemic effect on neurohormones, improved diastolic function. ACE inhibition was found to reduce net ACE activity and to increase plasma renin activity in aortic banded animals compared with untreated banded controls. There was also a trend for circulating noradrenaline levels to be increased at this stage of transition to failure in the untreated banded animals but ACE inhibition tended to restore the levels back to normal. In ACE inhibitor-treated animals, left ventricular (LV) diastolic pressure was significantly reduced, despite the persistent elevation of systolic pressure, but not yet restored completely to normal. In untreated, banded animals the transition to cardiac failure was evidenced as an increase in both systolic and diastolic dimensions with a reduction in fractional shortening.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed2002

Treatment of acromegaly improves myocardial abnormalities.

BACKGROUND: Treatment for acromegaly decreases left ventricular (LV) mass, but it is not clear whether diastolic dysfunction is also reversible. With Doppler echocardiography, before and after effective therapy, we assessed the LV morphology and function of patients with acromegaly who were free of complications. METHODS: In 15 patients with active acromegaly (age range, 33.4 +/- 9.3 years), we compared LV Doppler echocardiographic indices, before and after transsphenoidal surgery or radiotherapy or before and after both procedures, noting a significant drop in plasma levels of growth hormone (<2.0 ng/mL after oral glucose tolerance testing). Patients did not have arterial hypertension, diabetes mellitus, thyroid dysfunction, or coronary artery disease. Occasionally, in this series, patients had no symptoms of heart failure, and patients who underwent treatment with somatostatin analog drugs were not included because they did not have a significant hormonal drop. The follow-up period after hormonal control was 2.7 +/- 1.7 years. We also studied 15 healthy control subjects matched for age, sex, and body surface area. RESULTS: Patients with acromegaly compared with healthy control subjects had increased LV mass index, relative wall thickness, and deteriorated diastolic function. After therapy, most of the abnormalities improved: LV mass index (104 +/- 21 g/m(2) x 87 +/- 21 g/m(2); P <.01), LV relative wall thickness (0.40 +/- 0.06 x 0.35 +/- 0.04; P <.01), proto/telediastolic transmitral peak flow velocity ratio (1.17 +/- 0.33 x 1.49 +/- 0.34; P <.001), and isovolumetric relaxation period (126 +/- 18 ms x 113 +/- 13 ms; P <.05). CONCLUSION: Treatment of acromegaly in patients without clinical heart failure improves both LV morphology and diastolic function. Avoidance of progression to more advanced forms of acromegalic cardiomyopathy should be possible.

Acromegaly↗
PubMed2004

The pseudorestrictive pattern of transmitral Doppler flow pattern after conversion of atrial fibrillation to sinus rhythm: is atrial or ventricular dysfunction to blame?

Patients with paroxysmal atrial fibrillation (AF) who have recently converted from AF to sinus rhythm often exhibit a restrictive Doppler pattern in the transmitral flow (TMF) velocity. However, the mechanism of this phenomenon has not been well defined. We evaluated the temporal change of TMF pattern and hemodynamics after conversion of AF to in sinus rhythm in an animal model. Eight open-chest dogs underwent 3 hours of pacing-induced AF. TMF velocities and pressure data were acquired at baseline (sinus rhythm), immediately after conversion of AF, and every 10 minutes thereafter. Early diastolic TMF velocity was increased immediately after conversion and recovered to the baseline value in 20 minutes. Atrial systolic TMF velocity was reduced after AF and recovered to baseline value in 20 to 30 minutes. Early diastolic/atrial systolic TMF velocity was increased after conversion, and recovered to baseline value in 20 to 30 minutes. The mean left atrial (LA) pressure increased immediately, 10 and 20 minutes after the conversion of AF to sinus rhythm. The left ventricular end-diastolic pressure was increased and positive left ventricular dP/dt and tau were decreased immediately after AF, whereas they recovered within 10 minutes. In conclusion, a pseudorestrictive pattern of TMF after AF occurred as a result of transient LA mechanical functional impairment and increased LA pressure caused by LA stunning. Transient left ventricular diastolic dysfunction also effected the TMF velocity immediately after the conversion from AF to sinus rhythm, although it recovered faster than LA mechanical dysfunction.

Animals↗
PubMed2002

[Diagnosis of diastolic heart failure].

Fatigue and mainly dyspnea are symptoms the most often found in patients with diastolic heart failure. Flash pulmonary oedema is one of the most often found mode of clinical presentation. The heart has a normal size at chest X ray. Hemodynamic evaluation, the gold standard, shows increase in filling pressure but is not routinely performed. Doppler echocardiography has become the reference exam. It allows demonstrating: 1. the normal systolic function of the left ventricle (normal ejection fraction); 2. existence of a structural abnormality of the diastolic dysfunction; 3. calculating the level of pulmonary pressures. In the next years, it is likely that an increased plasma level of brain natriuretic peptide (BNP) becomes mandatory for a positive diagnosis.

Algorithms↗
PubMed2004

[Pulmonary hypertension, involvement of the right and left cardiac parts in patients with ankylosing spondylarthritis].

The literature states that pulmonary hypertension (PH) may develop in ankylosing spondylarthritis (AS); however, there are virtually no evidence for its incidence and the specific features of lesions of the right and left cardiac portions. This study was undertaken to determine the incidence of PH and its specific features in patients with AS. Fifty-five patients with AS were examined. There were prevalent patients with predominantly spinal lesions (50.9%), moderate progression of the disease (61.8%), and Grade III sacroileitis (49.1%). PH was detected in 70.96% of the patients, hypertrophy of the right ventricle (RV) was observed in 47.3%, RV dilation was in 34.5%. There were increases in the end systolic size and volume of the left ventricle (LV) in patients with AS (p < 0.05 and p < 0.05, respectively), ventricular septal thickening (p < 0.05), and a tendency for the posterior LV wall to be thickened. LV diastolic dysfunction occurred in 25.9% of the patients with AS. The found changes were interrelated with the duration of disease, the involvement of the vertebral column, the thoracic part in particular. Thus, the high incidence of PH was ascertained in patients with AS. The study confirms that echocardiography is of high informative value in the detection of PH and right cardiac changes in patients with AS, which shows this method to be screening in identifying the above pathology.

Adolescent↗
PubMed1994

[Old age from the viewpoint of the cardiologist].

The general cardiovascular performance of old people is determined by: a) inherent changes of the cardiovascular system which develop with age; b) delay of degenerative changes in some subjects caused by genetic factors, optimal physical activity and a proper diet; c) acquired diseases, in particular arteriosclerosis and hypertension. As a result of degenerative changes of the vascular wall the systolic pressure rises advancing age, some of the old people develop isolated systolic hypertension. Mild hypertrophy of the left ventricle develops also. The contracting ability of the heart muscle is preserved, the ejection fraction at rest and the cardiac output do not change. However, the diastolic function changes significantly-the elasticity of the left ventricle declines and its filling depends more on the atrial systole. A frequent cause of heart failure in old people is diastolic dysfunction. Pharmacotherapy of old people has some specific features which are discussed in more detail. A recent multicentre clinical investigation SHEP proved unequivocally, that effective treatment of systolic hypertension reduced in old people the risk of cerebrovascular attacks by 33%, of acute myocardial infarction by 27% and of cardiac failure by more than 50%! Based on these results it is clear that systolic hypertension must be treated equally systematically as diastolic hypertension. The approach to old people with cardiovascular disease must be strictly individual. Age alone must not be the reason for refusing access to the complete spectrum of modern diagnostic and therapeutic possibilities.

Aged↗
PubMed1999

[Doppler tissue imaging: a new method in the study of diastolic function in left ventricular hypertrophy].

BACKGROUND: Many factors influence diastolic function indexes obtained by monitoring left ventricular filling. Recent reports suggest that the study of myocardial wall velocity with Doppler tissue imaging (DTI) can give diastolic function parameters that are less affected by the same factors. An altered diastolic function has been demonstrated with invasive methods in patients with left ventricular hypertrophy (LVH). The aims of this study were 1) to compare a group of healthy subjects with a group of patients with LVH and presumably affected by diastolic dysfunction, to try to demonstrate if DTI could give new indexes to discriminate between the two groups; 2) to compare the indexes obtained with DTI against the ones given by Doppler study of left ventricular filling in the two populations. MATERIALS AND METHODS: Forty-two patients with LVH were compared to forty normal subjects. We studied the posterior wall velocity with pulsed DTI from parasternal view, measuring the early diastolic velocity (E'), the late diastolic velocity (A') and the E'/A' ratio. In addition, we estimated the usual ventricular filling parameters and the time interval between R wave of ECG and the peaks of E' and E waves. RESULTS: At left ventricular filling, patients with LVH showed an increase in A-wave peak velocity (mean 75.3 cm/s versus 66.4 cm/s; p < 0.05) and prolonged deceleration time (mean 216 ms versus 181 ms; p < 0.05), as compared to normal reference subjects. E-wave peak velocity and E/A ratio did not differ between the two groups. At DTI, patients with LVH had decreased early diastolic velocity (E') (mean 9 cm/s versus 12 cm/s; p < 0.05) and E'/A' ratio (mean 1.53 versus 1.91; p < 0.05) as compared to the control group. We observed an inverse correlation between E' wave and age in normal subjects. There was no correlation between the early diastolic myocardial velocity (E') and early inflow velocity (E) in both groups. A correlation was found between A and A' waves in normal subjects, but not in hypertrophic ones. The E'-wave peak always preceded the E-wave peak in all the subjects. CONCLUSION: Diastolic function indexes achieved by DTI can offer additional information that is independent of the data derived from left ventricular filling.

Adult↗