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Biomedical subjects

G M London

Publications and source records attributed to G M London.

At least 19 recordsLinked to original sources
PubMed2000

Postischemic vasodilation, endothelial activation, and cardiovascular remodeling in end-stage renal disease.

BACKGROUND: Cardiovascular complications are the major cause of death in end-stage renal disease (ESRD) patients. These complications are associated with concomitant cardiac and vascular remodeling, including left ventricular (LV) hypertrophy and hypertrophy of arterial walls. The endothelium influences the process of arterial remodeling. ESRD patients are characterized by the development of both cardiovascular remodeling and endothelial dysfunction. METHODS: Common carotid artery (CCA) intima-media thickness (IMT), CCA diameter, CCA distensibility, LV mass, and function were determined in 60 stable ESRD patients on hemodialysis and 34 age-, sex-, and blood pressure (BP)-matched controls, and their relationships with endothelial alterations were estimated by forearm postischemic vasodilation [flow debt repayment (FDR)] measured by venous plethysmography. We also evaluated the relationships between FDR and several cardiovascular risk factors or markers of inflammatory response or endothelial activation, for example, duration of dialysis, BP, smoking habits, cholesterol, parathormone (PTH), serum albumin, plasma fibrinogen, C-reactive protein (CRP), plasma homocysteine, plasminogen activator inhibitor (PAI-1), and von Willebrand factor (vWF). RESULTS: ESRD patients had increased LV mass, CCA diameter and CCA IMT, and had decreased CCA distensibility (P < 0.05). While the postischemic peak flow was comparable in controls and ESRD patients (29.2 +/- 9.1 vs. 27.9 +/- 0.2 mL/100 mL/min), FDR was lower in ESRD patients (116 +/- 31 vs. 88 +/- 32%, P < 0.001) because of the shorter duration of vasodilation (127 +/- 36 vs. 96 +/- 32 s, P < 0.001). The time to complete FDR was longer in ESRD patients (110 +/- 54 vs. 162 +/- 72 s, P < 0.001). ESRD patients had lower high-density lipoprotein cholesterol and serum albumin (P < 0.01) and higher triglycerides, fibrinogen, plasma homocysteine, vWF (P < 0.01), and PAI-1 (P < 0.05). For ESRD patients, significant negative age- and pressure-independent correlations were established between FDR and CCA diameter, duration of dialysis, and PAI-1. FDR was positively correlated with serum albumin. FDR and time to FDR were negatively correlated with CCA IMT and LV mass. CCA distensibility was positively associated with FDR (P < 0.001) and negatively with time to FDR (P < 0.001). The PAI-1 concentration was positively correlated with CCA IMT (P < 0.01) and negatively with CCA distensibility (P < 0.001). CONCLUSIONS: Our data provide the first evidence that cardiac and arterial remodeling in ESRD patients are inversely related to forearm reactive hyperemia. The diminished hyperemic response is due to the shorter duration of hyperemia and is associated with higher concentrations of serum markers of endothelial activation, suggesting that, in ESRD patients, endothelial dysfunction may be a factor influencing cardiovascular changes.

Adult↗
PubMed2000

Pathophysiology of cardiovascular disease in hemodialysis patients.

Cardiovascular disease is the principal cause of morbidity and mortality in dialysis patients. The principal alterations responsible are left ventricular hypertrophy and arterial disease characterized by an enlargement and hypertrophy of arteries and the high prevalence of atheromatous plaques. Left ventricular hypertrophy is the consequence of combined effects of chronic hemodynamic overload and nonhemodynamic biochemical and neurohumoral factors characteristic of uremia. The hemodynamic overload is due to flow and pressure overload. The flow overload is tightly related to hyperkinetic circulation caused by anemia, arteriovenous fistula, or overhydration and is characterized by an enlargement of the left ventricular cavity. The pressure overload in these patients is more tightly related to abnormal geometry and function of large conduit arteries, principally the stiffening of arterial tree. The flow overload is also in large part responsible for remodeling of arterial tree, and as the heart and vessels are a coupled interactive physiological system, cardiac and vascular alterations occur in parallel, being induced to a great extent by the same hemodynamic abnormalities. The principal clinical consequences of left ventricular hypertrophy and arterial alterations are heart failure, ischemic heart disease, and peripheral artery disease. Cardiovascular alterations are only partly reversible, and efforts should be directed toward early prevention.

Humans↗
PubMed2000

Arterial stiffening and vascular calcifications in end-stage renal disease.

BACKGROUND: Epidemiological studies have identified aortic stiffness as an independent predictor of cardiovascular mortality in end-stage renal disease (ESRD) patients. In these patients, aortic pulse wave velocity (PWV) was associated with mediacalcosis, but the influence of arterial calcifications on the viscoelastic properties of large arteries was not well characterized. The purpose of the present study was to analyse the influence of arterial calcifications on arterial stiffness in stable haemodialysed patients. METHODS: We studied 120 stable ESRD patients on haemodialysis. All patients underwent B-mode ultrasonography of common carotid artery (CCA), aorta, and femoral arteries to determine CCA distensibility, the elastic incremental modulus (Einc), and the presence of vascular calcifications. All patients underwent measurement of aortic PWV and echocardiogram. The presence of calcifications was analysed semiquantitatively as a score (0 to 4) according to the number of arterial sites with calcifications. RESULTS: Our observations indicate that arterial and aortic stiffness is significantly influenced by the presence and extent of arterial calcifications. The extent of arterial calcifications is in part responsible for increased left ventricular afterload, and is inversely correlated with stroke volume. The influence of calcifications is independent of the role of ageing and blood pressure. Arterial calcifications density increases with age, duration of haemodialysis, the fibrinogen level, and the prescribed dose of calcium-based phosphate binders. CONCLUSIONS: The results of this study showed that the presence of vascular calcifications in ESRD patients was associated with increased stiffness of large capacity, elastic-type arteries, like the aorta and CCA. The extent of arterial calcifications increased with the use of calcium-based phosphate-binders.

Adult↗
PubMed2000

Pathophysiology of anaemia: focus on the heart and blood vessels.

The amount of oxygen delivered to an organ depends on three factors: blood flow and its distribution; the oxygen-carrying capacity of the blood, i.e. haemoglobin concentration; and oxygen extraction. Non-haemodynamic and haemodynamic mechanisms operate to compensate for anaemia. Non-haemodynamic mechanisms include increased erythropoietin production to stimulate erythropoiesis, and increased oxygen extraction (displacement of the haemoglobin oxygen dissociation curve). This decreased affinity of oxygen for haemoglobin is mediated by increased 2,3-diphosphoglycerate concentrations. Increased cardiac output is the main haemodynamic factor, mediated by lower afterload, increased preload, and positive inotropic and chronotropic effects. Decreased afterload is due to vasodilatation and reduced vascular resistance as a consequence of lower blood viscosity, hypoxia-induced vasodilatation, and enhanced nitric oxide activity. Vasodilatation also involves recruitment of microvessels and, in the case of chronic anaemia, stimulation of angiogenesis. With decreased afterload, the venous return (preload) and left ventricular (LV) filling increase, leading to increased LV end-diastolic volume and maintenance of a high stroke volume and high stroke work. High stroke work is also due to enhanced LV contractility attributed to increased concentrations of catecholamines and non-catecholamine inotropic factors. In addition, heart rate is increased in anaemia, due to hypoxia-stimulated chemoreceptors and increased sympathetic activity. In the long term, these haemodynamic alterations lead to gradual development of cardiac enlargement and LV hypertrophy (LVH). The LVH is eccentric, characterized by increased LV internal dimensions and a normal ratio of wall thickness to cavity diameter, as occurs in other forms of volume overload. When anaemia-related LVH develops in an otherwise 'healthy' humoral environment, the lesions are reversible and the type of LVH is primarily physiological and is not associated with impaired diastolic function. In the absence of underlying cardiovascular disorders, severe anaemia (Haemoglobin concentration < 4-5 g/dl) leads to congestive heart failure. In the presence of heart disease, especially coronary artery disease, anaemia intensifies angina and contributes to a high incidence of cardiovascular complications. In end-stage renal disease (ESRD), LVH is influenced by many other factors, leading to intense interstitial fibrosis, to alterations in diastolic function, and usually to poor reversibility. The chronic increase in cardiac output contributes to arterial remodelling of central elastic arteries such as the aorta and common carotid artery. This remodelling consists principally of arterial enlargement and compensatory arterial intima--media thickening. In ESRD, these geometric changes are accompanied by arterial stiffening. The principal consequences of arterial alterations are increased systolic pressure and high inertia due to higher blood mass in the dilated arterial system. These alterations contribute to the development of LVH and abnormal coronary perfusion.

Anemia↗
PubMed2000

Therapeutic studies and arterial stiffness in hypertension: recommendations of the European Society of Hypertension. The Clinical Committee of Arterial Structure and Function. Working Group on Vascular Structure and Function of the European Society of Hypertension.

BACKGROUND: Increased pulse pressure and arterial stiffness are identified as predictors of cardiovascular risk in older hypertensive populations, particularly that of myocardial infarction. Because increased pulse pressure involves an increase in systolic (SBP) and a decrease in diastolic blood pressure (DBP), and because the former promotes cardiac hypertrophy and the latter alters coronary perfusion, a drug regimen reducing pulse pressure and decreasing arterial stiffness might further reduce cardiovascular risk. Under conventional treatment, normalization of DBP (< or = 90 mmHg) is not consistently associated with normalization of SBP (< or = 140 mmHg). THERAPEUTIC DESIGNS: In individuals older than 50 years, the goal of antihypertensive treatment should be, not only to decrease mean blood pressure (to less than 100 mmHg), but also to decrease pulse pressure (to less than 50 mmHg). Using appropriate pharmacological tools, trials should test whether an active decrease in arterial stiffness might produce an attenuation of the age-related increase in SBP and decrease in DBP, thus delaying the age-related increase in pulse pressure and decreasing further cardiovascular risk. This procedure requires concomitant non-invasive evaluations of aortic stiffness. CONCLUSION: The studies that are required in hypertension should use two different approaches: novel titrations of conventional drugs to achieve a decrease in either SBP or pulse pressure, and development of new drugs acting selectively on the large artery wall, to facilitate the conduct of subsequent controlled trials.

Antihypertensive Agents↗
PubMed2000

Alterations of arterial function in end-stage renal disease.

Cardiovascular disease is a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Epidemiological and clinical studies have shown that this is most frequently related to damage of large conduit arteries. Macrovascular disease develops rapidly in uremic patients and is responsible for the high incidence of ischemic heart disease, sudden death, peripheral artery diseases, and congestive heart failure. The most frequent causes of these complications are occlusive lesions due to atherosclerosis. Nevertheless, atherosclerosis, a disease characterized by the presence of plaques, represents only one form of structural response to metabolic and hemodynamic alterations which interfere with the process of aging, i.e., arteriosclerosis, characterized by dilation/hypertrophy and stiffening of arteries. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischemic lesions being the most characteristic consequence, the latter primarily disturbs the cushioning function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and hypertrophy of large conduit arteries and stiffening of arterial walls and represents a clinical form of accelerated aging process. The main clinical characteristics of arterial stiffening concern changes in blood pressure with isolated increase in systolic pressure and normal or lower diastolic pressure. The consequences of these alterations are: (1) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand and (2) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodeling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients.

Animals↗
PubMed2000

Stiffness of carotid artery wall material and blood pressure in humans: application to antihypertensive therapy and stroke prevention.

BACKGROUND AND PURPOSE: Because epidemiological studies show that increased pulse pressure and carotid wall-material stiffness are predictors of cardiovascular mortality independent of age, atherosclerosis, and conventional risk factors, the relationships between carotid wall stiffness and blood pressure are important to the optimization of cardiovascular prevention. SUMMARY OF REVIEW: In middle-aged hypertensive patients, mean and pulse pressures are increased, and systolic and diastolic pressures are increased to the same degree as mean pressure. Carotid hypertrophy is associated with normal wall stress, but no increased stiffness of wall material has been reported. With age, the normal wall stress is associated with a larger diameter and a stiffer material of carotid but not peripheral arteries. The stiffer wall involves calcifications, large amounts of collagen, and fragmentation and rupture of elastic tissue, which results in increased pulse-wave velocity and alterations of amplitude and timing of wave reflections and thus causes a disproportionate increase in systolic and pulse pressure. During this period, acutely administered nitrates in elderly subjects are able to reduce selectively systolic and pulse pressures without altering diastolic and mean blood pressure and composition of the carotid wall. CONCLUSIONS: New therapeutic approaches acting mainly on the wall of large arteries are needed to treat hypertension in elderly patients and prevent stroke and myocardial infarction. These drugs could either selectively lower pulse pressure through changes in wave reflections (as nitrates do) or decrease arterial wall stiffness through modification of the composition of material (such as compounds that act on collagen cross-linking).

Aging↗
PubMed1999

Impact of aortic stiffness on survival in end-stage renal disease.

BACKGROUND: Damage to large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased arterial stiffness and intima-media thickness, together with increased pulse pressure, are the principal arterial alterations. Whether increased aortic pulse-wave velocity (PWV), a classic marker of increased arterial stiffness, may predict all-cause and/or cardiovascular mortality has never been investigated. METHODS AND RESULTS: A cohort of 241 patients with ESRD undergoing hemodialysis was studied between April 1987 and April 1998. The mean duration of follow-up was 72+/-41 months (mean+/-SD). Mean age at entry was 51.5+/-16.3 years. Seventy-three deaths occurred, including 48 cardiovascular and 25 noncardiovascular fatal events. At entry, together with standard clinical and biochemical analyses, patients underwent echocardiography and aortic PWV measured by Doppler ultrasonography. On the basis of Cox analyses, 2 factors emerged as predictors of all-cause and cardiovascular mortality: age and aortic PWV. Hemoglobin and low diastolic pressure interfered to a smaller extent. After adjustment for all the confounding factors, an OR for PWV >12. 0 versus <9.4 m/s was 5.4 (95% CI, 2.4 to 11.9) for all-cause mortality and 5.9 (95% CI, 2.3 to 15.5) for cardiovascular mortality. For each PWV increase of 1 m/s in our study population, all-cause mortality-adjusted OR was 1.39 (95% CI, 1.19 to 1.62). CONCLUSIONS: These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.

Adult↗
PubMed1999

Influence of arterial pulse and reflected waves on blood pressure and cardiac function.

An integrated view of the role of arterial blood pressure in cardiovascular physiology should consider both the steady (mean blood pressure) and pulsatile (systolic, diastolic, and pulse pressures) components. This brief overview describes the important factors influencing these components, with emphasis on the consequences of arterial stiffening. In addition to their conduit function, arteries also perform a cushioning function that transforms the pulsatile flow generated by contraction of the left ventricle into steady flow at the periphery. Arterial compliance is a principal determinant of arterial blood pressure and is both pressure dependent and affected by vascular biomechanics. Other important factors that affect the steady and pulsatile components of blood pressure include ventricle performance, peripheral resistance, pulse wave velocity, and the timing of pulse wave reflections. Ageing and hypertension are important factors that contribute to reductions in arterial compliance. Important functional effects of this are that both the amplitude of the arterial pulse wave and pulse wave velocity increase, causing an early return of reflected waves from the periphery to the aorta. This may boost aortic and left ventricular pressures during systole at the expense of diastolic pressure, which is reduced. Studies have shown that stiffening of arteries and the associated increase in systolic and pulse pressures are important cardiovascular risk factors. Patients with an increased risk of cardiovascular events associated with such changes should be identified and receive appropriate therapeutic interventions.

Arteries↗
PubMed1999

Association of hyperphosphataemia with haemodynamic disturbances in end-stage renal disease.

BACKGROUND: Because recent data demonstrated that the shortened survival and excess cardiovascular death of end-stage renal disease (ESRD) patients are predicted by hyperphosphataemia, we examined the haemodynamic alterations associated with high serum phosphorus levels in ESRD patients on haemodialysis. METHODS: Sixty-six ESRD patients were studied. Patients were separated arbitrarily into two groups, i.e. with predialysis serum phosphate <2 mmol/l ('normal' phosphate) and, serum phosphate >2 mmol/l ('high' phosphate). Cardiac and arterial function and structure were analysed by computer-assisted ultrasonography. RESULTS: Hyperphosphataemic patients were characterized by higher diastolic and mean blood pressures (P<0.05), and higher cardiac index (P<0.001) caused by an increased stroke index (P<0.05) and higher heart rate (P<0.01). The cardiac work index was significantly increased in patients with higher phosphate levels (P<0.01). Hyperphosphataemic patients tended to have a higher common carotid artery diameter (P=0.07), but similar carotid artery intima-media thickness, and lower carotid wall-to-lumen ratio (P<0.05) than patients with 'normal' serum phosphorus. As a result of lower wall-to-lumen ratio in the presence of higher mean blood pressure, the carotid tensile stress was higher in hyperphosphataemic ESRD patients (P<0.05). CONCLUSION: These findings suggest that, in stable ESRD patients, hyperphosphataemia is associated with increased BP, hyperkinetic circulation, increased cardiac work, and high arterial tensile stress. These haemodynamic abnormalities could favour the development of cardiovascular complications and contribute to high cardiovascular morbidity and mortality.

Adult↗
PubMed1999

Influence of age and end-stage renal disease on the stiffness of carotid wall material in hypertension.

BACKGROUND: Incremental elastic modulus, which is the slope of the relationship between stress and strain of arterial vessels, is a marker of wall material stiffness. The radial artery incremental elastic modulus, which is not influenced by age, is normal or reduced in patients with essential hypertension but increased in patients with end-stage renal disease. Authors of studies on hypertension largely ignore the question of whether the incremental elastic modulus, measured in the common carotid artery as typical of a central artery site, differs according to age or to the presence of end-stage renal disease or both. SUBJECTS AND METHODS: The carotid incremental elastic modulus was measured in 208 hypertensive patients divided into four groups according to age (< or = or > 55 years) and the presence or absence of end-stage renal disease. The incremental elastic modulus was calculated from transcutaneous measurements of arterial internal diameter and wall thickness (echo-tracking device) and carotid pulse pressure (tonometry). Because the four groups of subjects had the same mean arterial pressure, the static incremental elastic modulus was calculated both in isobaric conditions and for the same wall stress. RESULTS: In nonuremic subjects, lumen diameter, wall thickness and the incremental elastic modulus were significantly (P < 0.001) increased in older subjects whereas compliance and distensibility were decreased. The mean (+/- SD) elastic modulus was 0.41 +/- 0.14 x 10(3) kPa in younger and 0.71 +/- 0.28 x 10(3) kPa in older subjects. In uremic subjects, the corresponding values were 0.48 +/- 0.30 and 0.90 +/- 0.49 x 10(3) kPa, and therefore higher than in nonuremic subjects, irrespective of age. Multiple regression analysis showed that age, mean arterial pressure and the presence of end-stage renal disease independently influenced carotid diameter, distensibility and the incremental elastic modulus. CONCLUSIONS: In hypertensive patients, the carotid incremental elastic modulus is increased independently in aging men and women and in the presence of uremia. This increase is not dependent on mechanical factors such as the level of mean blood pressure.

Adult↗
PubMed1999

Aortic pulse wave velocity as a marker of cardiovascular risk in hypertensive patients.

Large artery damage is a major contributory factor to cardiovascular morbidity and mortality of patients with hypertension. Pulse wave velocity (PWV), a classic evaluation of arterial distensibility, has never been ascertained as a cardiovascular risk marker. To determine the factors influencing aortic PWV and the potential predictor role of this measurement, we studied a cohort of 710 patients with essential hypertension. Atherosclerosis alterations (AA) were defined on the basis of clinical events. Calculation of cardiovascular risks, by use of Framingham equations, was performed in subjects without AA. PWV was higher in the presence of AA (14.9+/-4.0 versus 12.4+/-2.6 m/s, P<0.0001), even after adjustments on confounding factors and was the first determinant (P<0.0001) of the extent of atherosclerosis assessed as the sum of the atherosclerotic sites. In patients without AA, all cardiovascular risks increased constantly with PWV. Furthermore, at a given age, aortic PWV was the best predictor of cardiovascular mortality. The odds ratio of being in a high cardiovascular mortality risk group (>5% for 10 years) for patients in the upper quartile of PWV was 7.1 (95% confidence intervals 4.5 to 11.3). The presence of a PWV >13 m/s, taken alone, appeared as a strong predictor of cardiovascular mortality with high performance values. This study shows that aortic PWV is strongly associated with the presence and extent of atherosclerosis and constitutes a forceful marker and predictor of cardiovascular risk in hypertensive patients.

Age Factors↗
PubMed1999

Plasma homocysteine, aortic stiffness, and renal function in hypertensive patients.

Hyperhomocysteinemia has been associated with both vascular structure alterations and vascular clinical end points. To assess the relation between plasma homocysteine, structure and function of large arteries, and the presence of clinical vascular disease, we investigated a population of 236 hypertensive patients. We estimated arterial stiffness by measuring the carotid-femoral pulse wave velocity. Total plasma homocysteine was determined by fluorometric high-performance liquid chromatography. The presence of cardiovascular disease was defined on the basis of clinical events, including coronary heart disease, cerebrovascular disease, and peripheral vascular disease. In this population, pulse wave velocity was positively correlated with homocysteine, even after adjustments for age, mean blood pressure, extent of atherosclerosis, and creatinine clearance (P=0.016). Analysis of variance showed statistically significant differences between the mean values of homocysteine, creatinine clearance, and pulse wave velocity according to the extent of atherosclerosis, with an increase in these 3 parameters concomitant with an increase in the number of vascular sites involved with atherosclerosis. In conclusion, in hypertensive patients the levels of homocysteine are strongly and independently correlated to arterial stiffness measured by aortic pulse wave velocity. Plasma homocysteine, creatinine clearance, and aortic pulse wave velocity are higher in patients presenting with clinical vascular disease. These results suggest that the evaluation of aortic distensibility and homocysteine levels can help in cardiovascular risk assessment in hypertensive populations.

Adult↗
PubMed1999

Influence of arterial pulse and reflective waves on systolic blood pressure and cardiac function.

Hypertension is a cardiovascular risk factor classically attributed to a reduction in the calibre and/or number of small arteries and arterioles resulting in increased peripheral vascular resistance. The definition of blood pressure as a product of total peripheral resistance (TPR) and cardiac output, however, does not take into account the fluctuation of blood pressure and flow during the cardiac cycle, with systolic and diastolic blood pressure representing the extremes of pulse pressure fluctuations. Diastolic blood pressure is closer to mean blood pressure (and therefore to TPR) than systolic blood pressure, and as such has been used as a marker for the diagnosis of hypertension. However, this approach has no rational basis and was challenged by the Framingham Heart Study which demonstrated that systolic rather than diastolic blood pressure is a better risk marker for stroke and coronary artery disease in subjects aged 45 years and older. This view has subsequently been confirmed by several epidemiological and interventional studies. Systolic blood pressure is closely associated with pulse pressure and is determined by the pattern of left ventricular ejection, arterial stiffness and timing of arterial wave reflections, i.e. the geometrical and viscoelastic properties of large conduit arteries. In humans, with ageing and hypertension, the arteries stiffen as a result of progressive degeneration of the arterial media, increased collagen and calcium content, and dilation and hypertrophy of large arteries and the aorta. Thus, the increase in systolic blood pressure (as a result of arterial damage) increases the fatigue of arterial walls and accelerates arterial damage, producing a self-perpetuating cycle.

Blood Pressure↗
PubMed1998

Influence of body height on pulsatile arterial hemodynamic data.

OBJECTIVES: This study sought to present evidence that short stature is a hemodynamic liability, which could explain in part the inverse relation between body height and cardiovascular risk. BACKGROUND: Other explanations for the association of short stature with increased cardiovascular risk include advancing age, reduced pulmonary function, genetic factors, poor childhood nutrition and small-caliber coronary arteries. This study adds another factor-the physiologic effects of reduced body height on the arterial tree, which increase left ventricular work and jeopardize myocardial perfusion. METHODS: Four hundred two subjects were studied: 149 with end-stage renal disease and 253 with normal renal function. Measurements included blood pressure, body height, cardiac cycle length, carotid to femoral artery pulse wave velocity, carotid artery pulse waves (by applanation tonometry) and the arrival time of reflected waves. Calculations included the carotid augmentation index, carotid artery compliance and the diastolic to systolic pressure-time ratio (an index of myocardial supply and demand). RESULTS: On linear and stepwise multiple regression, body height correlated with all variables except mean blood pressure. CONCLUSIONS: The early systolic arrival of reflected waves in short people in this group acts to stiffen the aorta and increase the pulsatile effort of the left ventricle, even at the same mean blood pressures. Short stature also induces a faster heart rate, which increases cardiac minute work and shorten diastole. Stiffening lowers the aortic diastolic pressure and, coupled with a shortened diastole, could adversely influence myocardial supply. Although indirect, this evidence supports a physiologic hypothesis for the body height-cardiovascular risk association.

Adolescent↗