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PubMed1976

Reflection in the systemic arterial system: effects of aortic and carotid occlusion.

Experiments were performed in seven closed-chest anaesthetized male dogs to determine the role of pulse wave reflection in the pattern of flow and pressure in the ascending aorta. Ten days after implantation of an electromagnetic flow transducer around the ascending aorta a balloon catheter was placed in the descending aorta via the femoral arteries. At the same time a tip manometer was introduced into the ascending aorta. Aortic occlusions at three different sites caused pressure pulses with secondary systolic rises and flow pulses with biphasic deceleration. Secondary rises occurred 45 +/- 9.0 ms after the initial pressure rise for high aortic occlusion; this time was 75 +/- 8.5 ms for occlusion at the level of the diaphragm and 114 +/- 16.5 ms for occlusion near the level of the renal arteries. These times approximate the times in which the pulse travels from the tip manometer to the inflated balloons and back. Forward and reflected pressure and flow waves were calculated from reflection coefficients. Aortic occlusion caused larger reflected waves and the recorded wave forms were caused by the summation of forward and backward waves, the latter contributing the secondary pressure rise and the increased flow deceleration. Occlusion of both carotid arteries showed no specific reflection site but reflected waves were larger. This increased reflection can probably be explained as the result of greater total reflection from distributed sites under increased peripheral resistance.

Animals↗
PubMed1983

Turbulent blood flow in the ascending aorta of dogs.

A conical hot film anemometer probe was used to measure instantaneous velocities in the ascending aorta of anaesthetised, open-chest dogs. The probe was mounted on a saddle which allowed traversal of the aorta in 1 mm increments 4 cm above the aortic valve. From these point measurements, the radial distribution of velocity was obtained by averaging ten cardiac cycles. The contractile state of the heart was increased by sequential intravenous infusions of isoprenaline. The absolute peak centreline velocity in the baseline state ranged from 28 to 56 cm x s-1 and, in 20 micrograms x min-1 isoprenaline infusion, from 39 to 112 cm x s-1. Two major effects of isoprenaline on blood flow were noted: 1) isoprenaline dramatically increased peak centreline velocity, and 2) disturbances resembling turbulence appeared as peak velocity increased. With isoprenaline infusion disturbances existed throughout the deceleration portion of the aortic blood flow. Analysis of the frequency components of the velocity wave was performed, and significantly higher frequency components up to 100 Hertz were found in the turbulent cases compared to the laminar ones. Turbulent flow or disturbed flow is found when the ratio of Reynolds number to Womersley number is above 200. In general the hot film measurements showed that both laminar and disturbed velocity profiles tended to be flat throughout the cardiac cycle, with the sharp velocity gradient confined to the region of the wall. Turbulent normal stress during the deceleration portion of aortic blood flow were found in the orders of 15 to 30 dynes x cm-2 and the wall shear stresses were found to be from 10 dynes x cm-2 at the baseline condition to 50 dynes x cm-2 during the 20 micrograms x min-1 isoprenaline infusion.

Animals↗
PubMed1983

Differences between rabbit sinoatrial pacemakers in their response to Mg, Ca and temperature.

The rabbit sinoatrial node is functionally inhomogeneous with respect to its response to changes in Mg concentration (0.6 to 6.0 mmol X litre-1) and in Ca concentration (1.1 to 2.2 mmol X litre-1) and to changes in experimental temperature (30 to 38 degrees C). High Mg (6.0 mmol X litre-1) stabilises the position of the leading pacemaker. This pacemaker decelerates under high Mg, but the subsidiary ones decelerate even more. Consequently when a subsidiary pacemaker turns dominant--eg under low Ca or at low temperature--an enhanced chronotropic response to high Mg is observed. The superior (cranial) part of the rabbit sinoatrial node is more responsive to changes in Ca concentration than the inferior (caudal) part. The same holds true for changes in temperature.

Action Potentials↗
PubMed1992

Atrial contractility affects phasic blood flow velocity of atrial small vessels in the dog.

OBJECTIVES: The aim was to evaluate the relative contribution of atrial muscle contraction and atrial pressure to the phasic patterns of left atrial arterial and venous flows. METHODS: Using a laser Doppler velocimeter, blood velocities were measured in the atrial small arteries and veins (outer diameter: 150-500 microns) in anaesthetised open chest dogs (n = 21). The velocity sensor was fixed on the vessel surface with a drop of cyanoacrylate glue when good quality Doppler signals were consistently observed. Left atrial pressure and the contractility of the left atrium were changed by premature ventricular contraction and by intracoronary injection of isoprenaline (0.5 microgram), respectively. RESULTS: Premature ventricular contraction increased left atrial pressure significantly during arterial velocity measurements from 8.1(SD 2.7) to 16.4(1.3) mm Hg and during venous measurements from 8.2(1.2) to 14.3(3.7) mm Hg. However, premature ventricular contraction did not change the blood velocity patterns, the maximum deceleration rate of the systolic velocity wave in arteries, or the maximum acceleration rate of the systolic velocity wave in veins. Although isoprenaline did not change the left atrial pressure, it decreased minimum arterial blood velocity during atrial systole, from 3.3(3.4) to -2.5(3.2) cm.s-1, and increased maximum venous blood velocity from 15.9(5.5) to 19.2(7.4) cm.s-1. Isoprenaline also increased both the maximum arterial systolic velocity deceleration rate, from 90(45) to 234(143) cm.s-2, and the maximum venous systolic velocity acceleration rate from 356(230) to 763(366) cm.s-2. CONCLUSIONS: (1) Left atrial pressure is not a major determinant of the blood flow patterns of the atrial arteries and veins, and therefore it may not closely reflect pressure around mural vessels. (2) Atrial contractility affects the blood flow patterns of the atrial arteries and veins.

Animals↗
PubMed1993

Transmitral flow velocities and times during stress transthoracic echocardiography in patients with myocardial ischaemia.

Twenty-nine men with chronic stable angina pectoris were investigated using stress electrocardiography (ECG) and stress transthoracic echocardiography by means of transoesophageal stimulation of the left atrium. At rest and after each stimulated frequency, ECG and 2-dimensional echocardiography combined with Doppler were performed simultaneously. Fourteen patients without ischaemia at stress ECG and two patients who were subjected only to two different frequencies of stimulation were excluded from our study. Thirteen patients with ischaemic electrocardiographic response at stress, who were subjected to at least three stimulated frequencies, were evaluated. Their deceleration time of early transmitral filling was prolonged from 171 +/- 15.4 ms to 178.1 +/- 14.4 ms (P = ns) after the first stimulated frequency, to 172.8 +/- 15.1 ms after the second stimulated frequency (P = ns) and was shortened to 143.6 +/- 7.9 ms (P < 0.05) after the fastest stimulated frequency. The ratio of peak transmitral flow velocity in early diastole (E) to that during atrial contraction (A) decreased from 0.93 +/- 0.07 at rest to 0.85 +/- 0.07 (P < 0.05) after the first stimulated frequency, to 0.87 +/- 0.07 (P = ns) after the second stimulated frequency and increased to 1.13 +/- 0.08 (P < 0.05) after the fastest stimulated frequency. In patients with angina pectoris and myocardial ischaemia, the changes in the E/A ratio and deceleration time during stress are not linear and their direction depends on the moment of their evaluation. Their use for the quantitative evaluation of the diastolic function of the left ventricle is problematic.

Adult↗
PubMed2006

Effects of nebivolol in elderly heart failure patients with or without systolic left ventricular dysfunction: results of the SENIORS echocardiographic substudy.

AIMS: The SENIORS trial recently demonstrated that nebivolol reduces the composite risk of all-cause mortality and cardiovascular hospital admission in elderly patients with chronic heart failure and, importantly, that ejection fraction does not influence the clinical effects of nebivolol. An echocardiographic substudy was designed to evaluate the effects of nebivolol on systolic and diastolic left ventricular (LV) function in patients stratified according to the presence or absence of systolic LV dysfunction. METHODS AND RESULTS: The substudy randomized 112 patients in 29 European centres, of whom 104 were evaluable for the study; 43 had an ejection fraction (EF) 35%. LV end-systolic volume (ESV), EF, mitral valve E/A ratio, and E-wave deceleration time were assessed at baseline and after 12 months. Echocardiograms were submitted to a core laboratory to perform quantitative analysis in blinded condition. In the group with EF</=35%, nebivolol reduced ESV (adjusted difference between treatments 25.8 mL, 95%CI: -46.6; -5.0, P=0.016) and improved EF (adjusted difference between treatments 4.6%, 95%CI: 1.3;7.9, P=0.008); no changes were observed in the E/A ratio or E-wave deceleration time. In EF>35% group, no significant changes in either systolic or diastolic parameters were observed. CONCLUSION: In patients with heart failure and advanced systolic LV dysfunction, nebivolol reduces ventricular size and improves EF. The absence of detectable changes with standard echocardiography in patients with predominant diastolic heart failure questions the mechanism of benefit on morbidity/mortality in such patients.

Adrenergic beta-Antagonists↗
PubMed1994

Polygenic mutation in Drosophila melanogaster: estimates from response to selection of inbred strains.

Replicated divergent artificial selection for abdominal and sternopleural bristle number from a highly inbred strain of Drosophila melanogaster resulted in an average divergence after 125 generations of selection of 12.0 abdominal and 8.2 sternopleural bristles from the accumulation of new mutations affecting bristle number. Responses to selection were highly asymmetrical, with greater responses for low abdominal and high sternopleural bristle numbers. Estimates of VM, the mutational variance arising per generation, based on the infinitesimal model and averaged over the responses to the first 25 generations of selection, were 4.32 x 10(-3) VE for abdominal bristle number and 3.66 x 10(-3) VE for sternopleural bristle number, where VE is the environmental variance. Based on 10 generations of divergent selection within lines from generation 93, VM for abdominal bristle number was 6.75 x 10(-3) VE and for sternopleural bristle number was 5.31 x 10(-3) VE. However, estimates of VM using the entire 125 generations of response to selection were lower and generally did not fit the infinitesimal model largely because the observed decelerating responses were not compatible with the predicted increasing genetic variance over time. These decelerating responses, periods of response in the opposite direction to artificial selection, and rapid responses to reverse selection all suggest new mutations affecting bristle number on average have deleterious effects on fitness. Commonly observed periods of accelerated responses followed by long periods of stasis suggest a leptokurtic distribution of mutational effects for bristles.

Animals↗
PubMed1997

Age patterns of the life table aging rate for major causes of death in Japan, 1951-1990.

It has been widely supposed that human mortality from all causes increases with age nearly exponentially (at a constant rate) through adult ages except for very old ages, and that this exponential increase also holds fairly well for most major causes of death (CODs). However, the present analysis of death registration data for Japan, 1951-1990, reveals that the rate of age-related relative increase in mortality (the life table aging rate) changes with age significantly and systematically for many CODs. Above age 75, the mortality increase decelerates for most CODs; under age 75, it remains at a relatively stable pace for ischemic heart disease, decelerates for most major cancers, and accelerates for diseases related to a declining ability to maintain homeostasis (pneumonia, bronchitis, influenza, gastroenteritis, and heart failure). These results seem to suggest that significantly different types of senescent processes may underlie atherogenesis, oncogenesis, and immunosenescence.

Adult↗
PubMed2001

Array-based expression analysis of mouse liver genes: effect of age and of the longevity mutant Prop1df.

Ames dwarf mice, homozygous for the df allele at the Prop1 locus, live 40% to 70% longer than nonmutant siblings and represent the first single-gene mutant that extends life span in a mammal. To gain insight into the basis for the longevity of the Ames dwarf mouse, we measured liver mRNA levels for 265 genes in a group of 11 df/df mice, (three to four mice per age group), at ages 5, 13, and 22 months, and in 13 age- and sex-matched control mice. The analysis showed seven genes where the effects of age reach p < .01 in normal mice and six others with possible age effects in dwarf mice, but none of these met Bonferroni-adjusted significance thresholds. Thirteen genes showed possible effects of the df/df genotype at p < .01. One of these, insulin-like growth factor 1 (IGF-1), was statistically significant even after adjustment for multiple comparisons; and genes for two IGF-binding proteins, a cyclin, a heat shock protein, p38 mitogen-activated protein kinase, and an inducible cytochrome P450 were among those implicated by the survey. In young control mice, half of the expressed genes showed SDs that were more than 58% of the mean, and a simulation study showed that genes with this degree of interanimal variation would often produce false-positive findings when conclusions were based on ratio calculations alone (i.e., without formal significance testing). Many genes in our data set showed apparent young-to-old or normal-to-dwarf ratios above 2, but the large majority of these proved to be genes where high interanimal variation could create high ratios by chance alone, and only a few of the genes with large ratios achieved p < .05. The proportion of genes showing relatively large changes between 5 and 13 months, or from 13 to 22 months of age, was not diminished by the df/df genotype, providing no support for the idea that the dwarf mutation leads to global delay or deceleration of the pace of age-dependent changes in gene expression. These survey data provide the foundation for replication studies that should provide convincing proof for age- and genotype-specific effects on gene expression and thus reveal key similarities among the growing number of mouse models of decelerated aging.

Aging↗
PubMed2004

Establishing an appropriate ethical framework: the moral conversation around the goal of prolongevity.

This article presents a triadic framework for ethical discourse around the biogerontological goal of prolongevity, which might someday become achievable through the deceleration of aging. The methods are those of the humanities and philosophical analysis. The perspectives of natural law, equalitarian justice, and beneficence are presented in a balanced manner, although the conclusion reached is that the goal of prolongevity through decelerated aging is ethically valid as a potential means to the beneficent amelioration of the many diseases for which old age is the major susceptibility factor.

Aged↗
PubMed1989

Age differences in heart rate patterns during concentration in a precision sport: implications for attentional functioning.

Highly skilled young (M = 29.5 years) and older (M = 50.0 years) miniature golf players were observed in relaxed training and high-arousal competition rounds. Motor performance (number of shots), subjective ratings of anxiety, and heart rate were registered. Results showed a similar increase of arousal from training to competition for both age groups. However, the older group deteriorated in motor performance from training to competition, whereas the younger group played equally well on both occasions. Results from continuous measurement of heart rate indicated a deceleration during the concentration phases among the younger players, and the magnitude of deceleration increased from training to competition. In contrast, heart rate accelerated during training among the older players, the magnitude of the heart rate change decreasing from training to competition. This evidence suggests that the deterioration in motor performance observed in older players in stressful competitive activity may be due to age-related changes in attentional functioning.

Adult↗
PubMed2006

Identifying cytoplasmic input to the cell wall of growing Chara corallina.

Plants enlarge mostly because the walls of certain cells enlarge, with accompanying input of wall constituents and other factors from the cytoplasm. However, the enlargement can occur without input, suggesting an uncertain relationship between cytoplasmic input and plant growth. Therefore, the role of the input was investigated by quantitatively comparing growth in isolated walls (no input) with that in living cells (input occurring). Cell walls were isolated from growing internodes of Chara corallina and filled with pressurized oil to control turgor pressure while elongation was monitored. Turgor pressure in living cells was similarly controlled and monitored by adding/removing cell solution. Temperature was varied in some experiments. At all pressures and temperatures, isolated walls displayed turgor-driven growth indistinguishable in every respect from that in living cells, except the rate decelerated in the isolated walls while the living cells grew rapidly. The growth in the isolated walls was highly responsive to temperature, in contrast to the elastic extension that has been shown to be insensitive to similar temperatures. Consequently, strong intermolecular bonds were responsible for growth and weak bonds for elastic extension. Boiling the walls gave the same results, indicating that enzyme activities were not controlling these bonds. However, pectin added to isolated walls reversed their growth deceleration and returned the rate to that in the living cells. The pectin was similar to that normally produced by the cytoplasm and deposited in the wall, suggesting that continued cytoplasmic input of pectin may play a role in sustaining turgor-driven growth in Chara.

Cell Enlargement↗
PubMed1995

The value of different resistance parameters in distinguishing biopsy-proved dysfunction of renal allografts.

The data concerning the value of duplex sonography in diagnosing parenchymatous renal allograft dysfunction are controversial. Most early studies did not take into consideration the many factors influencing resistance parameters. We therefore performed a prospective, biopsy-controlled study with exclusion of all known sources of error regarding resistance parameters. Furthermore we investigated the value of a new resistance parameter, the systolic deceleration percentage. Forty-seven duplex sonographic studies were performed on 43 patients (30 male, 13 female, median age 47 years, range 7-70). Fourteen studies were done on normally functioning grafts (control group) an average of 33 days after transplantation. Thirty-three studies were performed on dysfunctional grafts immediately prior to biopsy. Grafts which had been transplanted more than a year previously or with vascular findings or any other clinical or sonographic pathology probably explaining function deterioration were excluded. In all patients, the resistive index (RI), pulsatility index (PI) and systolic deceleration percentage (DP) were calculated in the main renal artery and in the interlobar artery. Of the 33 grafts with dysfunction, nine had vascular rejection (VR), 11 interstitial rejection (IR), 11 cyclosporin A toxicity (CAT) and two other histologies (OR). The mean RI in normal grafts (NO) was 0.71 +/- 0.06 in the main artery and 0.68 +/- 0.06 in the interlobar artery, in VR 0.86 +/- 0.12 and 0.80 +/- 0.18, in IR 0.72 +/- 0.05 and 0.70 +/- 0.07, in CAT 0.67 +/- 0.06 and 0.65 +/- 0.07 and in OR 0.64 +/- 0.07 and 0.60 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Is stroke mortality on the decline in England?

This paper challenges the assumption that mortality from stroke will remain constant or decline over the next few decades. A decline in stroke mortality could be brought about by changes in factors acting close to the time of death (period effect) or by risk factors determined by the generation into which a person is born (cohort effect). Age-specific death rates for stroke (1931-1985) in England and Wales were analyzed to estimate the influence of these different effects. There were significant effects for age, period, and cohort on mortality from stroke with significantly different age and period effects in each sex. The effect of age was linear, with an increasing mortality with age in both sexes. Cohort analysis demonstrated a deceleration away from the previous trend in the mortality rates associated with birth cohorts born after 1880, followed by an acceleration in the trend of mortality rates in cohorts born after 1910. These relative increases in risk for cohorts born after 1910 were offset by a deceleration in mortality associated with periods from around 1951-1954. Since cohort effects are likely to be associated with a lifetime increase in risk of stroke mortality, it is difficult to predict the extent of any long-term fall in stroke incidence.

Adult↗
PubMed1997

Atrial conduction abnormalities in patients with systemic progressive sclerosis.

BACKGROUND: Atrial abnormalities in patients with progressive systemic sclerosis have not been evaluated in terms of intra-atrial conduction. We hypothesized that a delay in atrial conduction in these patients might produce diastolic abnormalities as well as atrial arrhythmias. OBJECTIVE: To evaluate the atrial function of patients with progressive systemic sclerosis by using echocardiography to measure the intra-atrial electromechanical activation coupling interval. METHODS: Twenty patients with progressive systemic sclerosis were assessed by Doppler echocardiography. Twenty age-matched healthy controls were also evaluated. Two-dimensional guided M-modes of ventricular long axes were recorded using simultaneous phono- and electrocardiograms of the apical four chamber view at the right lateral, septal and left lateral sites of the atrioventricular rings. Transmitral and tricuspid pulsed Doppler flow velocities were also recorded. Filtered P wave duration was measured on the signal averaged ECG to determine the duration of atrial electrical activation. RESULTS: There was a delay in P on the electrocardiogram (P) at the onset of atrial contraction on long axis M-modes at all three atrioventricular ring sites in patients with progressive systemic sclerosis as compared with controls (P-right; 56 +/- 13 vs 47 +/- 10 ms, P-septal; 74 +/- 14 vs 55 +/- 10 ms, and P-lateral; 93 +/- 16 vs 72 +/- 11 ms, P < 0.01). Inter-atrial conduction time [(P-lateral)-(P-right)] was delayed in patients with progressive systemic sclerosis, compared with healthy controls (37 +/- 15 vs 25 +/- 6 ms, P < 0.01). Mitral A waves acceleration and deceleration times were also decreased in the patients. The interval was prolonged between P to the onset and the peak of the A wave in transmitral flow. Duration of the filtered P wave was significantly prolonged in progressive systemic sclerosis as compared with controls (124 +/- 12 ms vs 106 +/- 8 ms, P < 0.01). PQ intervals, E waves and acceleration and deceleration times did not differ significantly in progressive systemic sclerosis vs, controls. The A wave acceleration rate on transmitral flow (peak A wave velocity/acceleration time) showed a significant correlation with inter-atrial conduction delay (r = 0.55, P < 0.01). CONCLUSIONS: Intra-atrial electromechanical coupling intervals were delayed in patients with progressive systemic sclerosis. Thus, the mechanical late diastolic filling time due to atrial contraction in the total diastolic phase was severely limited, and this resulted in a restricted mitral A wave. We should therefore evaluate patients with progressive systemic sclerosis for significant atrial abnormalities.

Atrial Function↗
PubMed1990

Pulsed Doppler evaluation of left ventricular filling in subjects with pathologic and physiologic third heart sound.

Haemodynamic studies suggest that the rapid deceleration of left ventricular inflow at the end of early diastole may play an important role in the genesis of the third heart sound (S3). To confirm this hypothesis noninvasively, pulsed Doppler of transmitral flow was used. Mitral flow velocity wave was recorded in 20 post-infarction patients with audible S3 (Group 1), in 20 young healthy individuals with physiologic S3 (Group II), in 20 postinfarction patients without S3 (Group III) and in 20 normal adults (Group IV). Peak flow velocity in early diastole (Ev), peak flow velocity during atrial systole (Av), the Ev/Av ratio, the deceleration of early diastolic flow (EF slope), the ratio of the time velocity integral of early diastole to the total time velocity integral (TVle/TVlt) and the isovolumic relaxation time (IVRT) were measured from Doppler recordings. The time relation between S3, the mitral valve motion on M-mode tracing, and the mitral flow velocity wave were analysed comparing the intervals from the second sound to Ev (A2-Ev), to the E point of mitral valve motion (A2-Em) and to the S3 (A2-S3). In groups I and II Ev/Av ratio was higher (respectively 4.4 +/- 2.2 and 2.8 +/- 1.1) than in group III (0.8 +/- 0.4) and IV (1.3 +/- 0.3). Similar results were found for the TVle/TVlt ratio. In both groups with S3, EF slope was significantly steeper (respectively 9 +/- 1.8 and 7.5 +/- 1.1 m s) than in normal adults (4.4 +/- 1.1 m s) and patients without S3 (3.6 +/- 1.1 m s).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Prevalence and determinants of left ventricular diastolic filling abnormalities in an unselected hypertensive population.

The independent contribution of age, sex, duration of hypertension, heart rate, clinic and ambulatory blood pressure and echocardiographic left ventricular mass to left ventricular diastolic filling abnormalities in essential hypertension was investigated in 250 subjects (145 untreated and unselected hypertensives and 105 healthy normotensive controls) undergoing Doppler and standard echocardiography and non-invasive 24-h ambulatory blood pressure monitoring. Late and early diastolic transmitral peak flow velocities and their ratio (all P less than 0.01), the rate of deceleration of early diastolic mitral flow (P less than 0.01) and the time of deceleration of early diastolic mitral flow (P = 0.018) were abnormal in the hypertensive group vs controls. None of these parameters significantly varied in the presence vs absence of LV hypertrophy. In the hypertensive group, the prevalence of abnormal age-corrected Doppler values varied up to 46% (up to 45.4% and 50% in the absence and presence of left ventricular hypertrophy, respectively; P = n.s.). In a stepwise multivariate regression analysis, age and average daytime or night-time ambulatory blood pressure showed a significant independent relationship with each of these Doppler indexes of left ventricular diastolic filling. Late transmitral peak flow velocity and the ratio of late to early peak flow velocity were also independently affected by the heart rate. Sex, duration of hypertension, clinic systolic and diastolic blood pressure and left ventricular mass index did not show any independent relationship to these Doppler parameters of left ventricular filling. In conclusion, Doppler abnormalities of diastolic transmitral blood flow were detected in up to 46% of patients in an unselected hypertensive population with a low prevalence (14.5%) of left ventricular hypertrophy. Age and ambulatory blood pressure, but not sex, duration of hypertension, clinic blood pressure and left ventricular mass itself, were the major independent determinants of these abnormalities.

Aged↗
PubMed1996

Left ventricular function in scleroderma.

Scleroderma affects the left heart directly and indirectly via the effects of systemic hypertension. Using transthoracic echocardiography, we evaluated 35 patients with scleroderma and compared them with matched control subjects. Compared with controls, there were no differences between left ventricular dimensions, wall thickness, calculated mass or fractional shortening. However, the left atrium was enlarged (P = 0.006) and the mitral deceleration time was prolonged (P = 0.0005) in patients with scleroderma; suggesting abnormal diastolic function. After adjusting for potential confounders, duration of Raynaud's was found to be an independent predictor of deceleration time (P = 0.04), E/A peak velocity ratio (P = 0.04), A peak velocity (P = 0.004) and A velocity time integral (P = 0.0001), all measures of diastolic function. This group of individuals with scleroderma have evidence of abnormal diastolic function of the left ventricle despite normal left ventricular size and systolic function, and in the absence of hypertrophy. This finding is independent of the use of vasoactive medications and history of systemic hypertension, and thus may be due to primary myocardial involvement by scleroderma. The tendency to abnormal diastolic function of the left ventricle correlated with the duration of Raynaud's phenomenon.

Adolescent↗