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PubMed1999

Angiotensin IV has mixed effects on left ventricle systolic function and speeds relaxation.

OBJECTIVE: A novel angiotensin receptor has been described and named AT4. Ligands for this receptor include the angiotensin II (Ang II) metabolite Ang II (3-8), known as angiotensin IV (Ang IV). There is 10-fold more AT4 receptor than AT1 receptor in rabbit myocardium. The AT4 receptor has a high affinity for Ang IV (Ki in rabbit myocardium < 2 x 10(-9)) and similar ligands, but very low affinity for Ang II (Ki in rabbit myocardium > 10(-6)). Although several functions have been attributed to the novel Ang IV peptide/AT4 receptor system, the effect of this system on left ventricular (LV) function has not been studied. We hypothesized (1) that Ang IV would affect LV function and (2) that any effects would be opposite to those of Ang II. METHODS: Using the buffer-perfused (30 degrees C) isolated rabbit heart, we studied the effect of the AT4 agonist Nle1-Ang IV on LV systolic function, quantified using both Frank-Starling and end-systolic pressure-volume relationships, and relaxation. We also studied the effect of the AT1/AT2 agonist, Sar1-Ang II on LV function. Finally, because the profile of effect of Nle1-Ang IV was similar to the reported effect of nitric oxide (NO), we also studied the effect of Nle1-Ang IV in the presence of the NO synthase inhibitor NG-monomethyl-L-arginine. RESULTS: Nle1-Ang IV reduced LV pressure-generating capability at any volume but increased the sensitivity of pressure development to volume change. Nle1-Ang IV reduced LV ejection capability. Sar1-Ang II had the opposite effect-increasing both pressure generation and ejection capability. Finally, both Sar1-Ang II and Nle1-Ang IV speeded LV relaxation. Inhibition of NO synthase did not alter the effect of Nle1-Ang IV on LV systolic function or relaxation. CONCLUSIONS: AT4 receptor agonism has mixed effects on LV systolic function, depressing pressure-generation and ejection capabilities, but enhancing the sensitivity of pressure development to volume change. It also speeds relaxation. The effect of Ang IV on systolic function is generally opposite to the effect of Ang II, whereas the Ang IV influence on relaxation is similar to the effect of Ang II.

Adrenergic beta-Antagonists↗
PubMed1997

Influence of basal release of nitric oxide on systolic and diastolic function of both ventricles.

Nitric oxide is continuously released by coronary artery endothelium under basal conditions; it maintains vascular tone and regulates coronary blood flow. The objective of this study was to investigate the influence of this basal release of nitric oxide on right and left ventricular systolic and diastolic function. Isolated pig hearts perfused at a constant pressure with enriched autologous blood were used. Systolic and diastolic pressure-volume relationships of isovolumically contracting hearts were studied in the control setting and after addition of 1 mmol/L L-N(G)-monomethyl-arginine followed by 5 mmol/L L-arginine to the perfusate. Addition of L-N(G)-monomethyl-arginine caused an acute rise in coronary vascular resistance and a reduction in right and left ventricular systolic function as evaluated by the slope values of the pressure-volume curves, but had little effect on the diastolic function of either ventricle. L-Arginine restored the systolic function to the control level. This alteration in ventricular function was not a result of ischemia because myocardial oxygen consumption was not significantly affected by the acute increase in coronary vascular resistance induced by L-N(G)-monomethyl-arginine. We conclude that basal release of nitric oxide has no direct negative inotropic effect, but in fact plays an important role in preserving right and left ventricular systolic function and maintains the basal coronary vascular tone.

Animals↗
PubMed2003

Efficacy of angiotensin-converting enzyme inhibitors and beta-blockers in the management of left ventricular systolic dysfunction according to race, gender, and diabetic status: a meta-analysis of major clinical trials.

OBJECTIVES: This study sought to assess the effect of angiotensin-converting enzyme (ACE) inhibitors and beta-blockers on all-cause mortality in patients with left ventricular (LV) systolic dysfunction according to gender, race, and the presence of diabetes. BACKGROUND: Major randomized clinical trials have established that ACE inhibitors and beta-blockers have life-saving benefits in patients with LV systolic dysfunction. Most patients enrolled in these trials were Caucasian men. Whether an equal effect is achieved in women, non-Caucasians, and patients with major comorbidities has not been established. METHODS: The authors performed a meta-analysis of published and individual patient data from the 12 largest randomized clinical trials of ACE inhibitors and beta-blockers to produce random effects estimates of mortality for subgroups. RESULTS: Data support beneficial reductions in all-cause mortality for the use of beta-blockers in men and women, the use of ACE inhibitors and some beta-blockers in black and white patients, and the use of ACE inhibitors and beta-blockers in patients with or without diabetes. Women with symptomatic LV systolic dysfunction probably benefit from ACE inhibitors, but women with asymptomatic LV systolic dysfunction may not have reduced mortality when treated with ACE inhibitors (pooled relative risk = 0.96; 95% confidence interval: 0.75 to 1.22). The pooled estimate of three beta-blocker studies supports a beneficial effect in black patients with heart failure, but one study assessing bucindolol reported a nonsignificant increase in mortality. CONCLUSIONS: Angiotensin-converting enzyme inhibitors and beta-blockers provide life-saving benefits in most of the subpopulations assessed. Women with asymptomatic LV systolic dysfunction may not achieve a mortality benefit when treated with ACE inhibitors.

Adrenergic beta-Antagonists↗
PubMed1984

Left ventricular end-systolic wall stress-velocity of fiber shortening relation: a load-independent index of myocardial contractility.

The velocity of circumferential fiber shortening (Vcf) is an index of myocardial performance which, although sensitive to contractile state, has limited usefulness because of its dependence on left ventricular loading conditions. This study investigated the degree and velocity of left ventricular fiber shortening as it relates to wall stress in an attempt to develop an index of contractility that is independent of preload and heart rate while incorporating afterload. Studies were performed in 78 normal subjects using M-mode echocardiography, phonocardiography and indirect carotid pulse tracings under baseline conditions. In addition, studies were performed on 25 subjects during afterload augmentation with methoxamine, 8 subjects before and during afterload challenge after increased preload with dextran and 7 subjects with enhanced left ventricular contractility with dobutamine. The relation of end-systolic stress to the velocity of fiber shortening and to the rate-corrected velocity of shortening (corrected by normalization to an RR interval of 1) was inversely linear with correlation coefficients of -0.72 and -0.84, respectively. Alterations in afterload, preload or a combination of the two did not significantly affect the end-systolic wall stress/rate-corrected velocity of shortening relation, whereas during inotropic stimulation, the values were higher, with 94% of the data points above the normal range. Age did not appear to affect the range of normal values for this index. In contrast, the end-systolic wall stress/fractional shortening relation was not independent of preload status, responding in a manner similar to that seen with a positive inotropic intervention. Thus, the velocity of circumferential fiber shortening normalized for heart rate is inversely related to end-systolic wall stress in a linear fashion. Accurate quantitation can be performed by noninvasive means and a range of normal values determined. This index is a sensitive measure of contractile state that is independent of preload, normalized for heart rate and incorporates afterload. In contrast, the end-systolic wall stress/fractional shortening relation is dependent on end-diastolic fiber length in the range of physiologically relevant changes in preload.

Adolescent↗
PubMed1985

Plasma epinephrine concentration in healthy men: correlation with systolic pressure and rate-pressure product.

Relations among plasma epinephrine, norepinephrine and renin activity and systolic pressure, diastolic pressure, heart rate and the product of heart rate and systolic pressure (rate-pressure product) were evaluated in 31 healthy men whose arterial pressure spanned the range from normal to mildly elevated. Measurements were made during 60 minutes with the patient in the supine position and during 10 minutes of quiet standing. In the supine position, highly significant regressions were found between systolic pressure or rate-pressure product and plasma epinephrine, but not between these variables and norepinephrine or renin activity. A weakly significant correlation was also found between heart rate and norepinephrine. On standing, norepinephrine and epinephrine increased significantly. In this position, rate-pressure product was significantly related by regression analysis only with plasma epinephrine. Weakly significant correlations between systolic pressure and epinephrine and between heart rate and norepinephrine and epinephrine were also found. Plasma renin activity was not significantly correlated with arterial pressure, heart rate or rate-pressure product in either position. These results suggest that plasma epinephrine is a determinant of systolic pressure when postural reflexes are minimized and that epinephrine may participate in control of cardiac work load, as reflected by rate-pressure product in the absence of exercise or definable stress.

Adolescent↗
PubMed1985

Accuracy of radionuclide ventriculography for estimation of left ventricular volume changes and end-systolic pressure-volume relations.

Estimation of left ventricular end-systolic pressure-volume relations depends on the accurate measurement of small changes in ventricular volume. To study the accuracy of radionuclide ventriculography, paired radionuclide and contrast ventriculograms were obtained in seven dogs during a control period and when blood pressure was increased in increments of 30 mm Hg by phenylephrine infusion. The heart rate was held constant by atropine infusion. The correlation between radionuclide and contrast ventriculography was excellent. In the individual animals, the average r value for left ventricular volume was 0.96 +/- 0.03 (+/- SD) (p = 0.001, n = 7) and the mean r value for end-systolic volume changes was 0.90 +/- 0.08 (n = 7, range 0.76 to 0.99). For the entire series, there were 33 end-systolic volume changes, and there was an equally strong radionuclide-contrast correlation (r = 0.89, p less than 0.001, n = 33), even though the volume changes averaged only 11.9 +/- 8.2 ml (range 0.3 to 38.1). The systolic pressure-volume relations were linear for both radionuclide and contrast ventriculography (r = 0.98 and 0.97, respectively, n = 7). The mean slope for radionuclide ventriculography (2.9 +/- 1.4) was lower than the mean slope for contrast ventriculography (4.8 +/- 1.7) (p = 0.004); however, the slopes correlated well (r = 0.81, n = 7, p = 0.026). The radionuclide-contrast volume relation was compared using background subtraction, attenuation correction, neither of these or both. By each method, radionuclide ventriculography was valid for measuring small changes in left ventricular volume and for defining end-systolic pressure-volume relations.

Animals↗
PubMed1987

End-systolic radius to thickness ratio: an echocardiographic index of regional performance during reversible myocardial ischemia in the conscious dog.

Regional myocardial dysfunction induced by ischemia is associated with less thickening and a larger ventricular radius at end-systole. Thus, end-systolic radius to thickness ratio measured by echocardiography may provide an accurate index of regional left ventricular function that is totally independent of cardiac motion. To test this hypothesis, a total of 14 transient (less than or equal to 10 minutes) coronary artery occlusions (8 left anterior descending, 6 left circumflex) followed by up to 24 hours of reperfusion were performed in six chronically instrumented conscious dogs providing multiple grades of regional ventricular dysfunction. Regional myocardial thickening fraction was determined with epicardial pulsed Doppler probes and served as an independent standard for comparison with simultaneous echocardiographic measurements. End-systolic radius to thickness ratio and radial shortening fraction were derived from the two-dimensional echocardiographic short-axis view along 12 equidistant radii. In the ischemic zone, percent thickening fraction averaged 22 +/- 5% during baseline, decreased to -4 +/- 4% during occlusion with gradual return to baseline after reperfusion. End-systolic radius to thickness ratio averaged 1.39 +/- 0.25 before coronary occlusion and increased to 2.97 +/- 0.48 during occlusion with a gradual return to baseline values. A significant correlation was found between Doppler-determined thickening fraction measurements and echocardiographic end-systolic radius to thickness ratio as well as radial shortening fraction for absolute values (r = -0.83 and 0.75, respectively; n = 65) and percent change from baseline (r = -0.86 and 0.78, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Effect of myocardial hypertrophy on systolic and diastolic function in children: insights from the force-frequency and relaxation-frequency relationships.

OBJECTIVE: The objective of this study was to evaluate the effect of myocardial hypertrophy on systolic and diastolic properties of the left ventricle in children. BACKGROUND: In children with myocardial hypertrophy, ejection phase indices are invariably increased. However, indices of force-generation, e.g., end-systolic elastance and invasive indices of diastolic properties, have been studied infrequently in children with myocardial hypertrophy. METHODS: We studied 10 children with congenital aortic stenosis or coarctation of aorta and nine control patients. Systolic properties were assessed from shortening fraction, end-systolic fiber elastance (Ef(es)) measured at resting heart rates, and force-frequency relationship measured at heart rates increasing from 110 to 160 beats per minute. Diastolic properties were assessed from time constant of relaxation (tau) at matched heart rates, chamber stiffness constant, myocardial stiffness constant, and relaxation-frequency relationship measured at gradually increasing heart rates. RESULTS: Ef(es) remained unchanged by myocardial hypertrophy, however, tau was prolonged (tauL: 27.3+/-2.3 vs. 21.8+/-2.2 ms, p < 0.001; and tauD: 43.2+/-3.1 vs. 34.3+/-3.3 ms, p < 0.001). Both chamber and myocardial stiffness constants remained unchanged. Incremental increases in heart rate produced incremental improvement in both contraction and relaxation. Slopes of force-frequency and relaxation-frequency relationships remained unchanged in the experimental group. However, the relaxation-frequency relationship manifested a parallel shift upward. CONCLUSIONS: In conscious, sedated children with myocardial hypertrophy, systolic function assessed by an index of force generation remains unchanged. However, relaxation is prolonged but passive diastolic properties remain unaffected. The combined effect of hypertrophy and heart rate does not alter the force-frequency and relaxation-frequency relationships.

Aortic Coarctation↗
PubMed2004

Initial clinical evaluation of cardiac systolic murmurs in the ED by noncardiologists.

It is not exactly known how ED physicians perform in evaluating cardiac systolic murmurs. In 203 consecutive medical ED patients with systolic murmur, we compared the initial clinical evaluation, including auscultation, with transthoracic echocardiography. Of the 203 patients, 132 (65%) had innocent murmurs and 71 patients (35%) had valvular heart disease. Sensitivity and specificity of the initial clinical routine evaluation in diagnosing echocardiographic valvular heart disease were 82% (70%-86%) and 69% (60%-76%), respectively. Independent significant positive predictors of valvular heart disease were grade >2/6 systolic murmur (odds ratio [OR], 8.3; confidence interval [CI], 3.5-19.7, P<.001) and pathologic electrocardiogram (ECG) (OR, 8.4; CI, 3.2-22, P<.001. Patients younger than 50 years with a systolic murmur graded < or =2/6 had innocent murmurs in 98%. The initial clinical evaluation, including auscultation, by experienced ED physicians in internal medicine distinguishes well between innocent murmurs and valvular heart disease in medical patients with cardiac systolic murmurs.

Adolescent↗
PubMedDate not supplied

Dynamics of systolic pulmonary venous flow in mitral regurgitation: mathematical modeling of the pulmonary venous system and atrium.

The noninvasive assessment of mitral regurgitation has been an elusive clinical goal. Recent studies have highlighted the value of pulmonary venous (PV) flow reversal in indicating the presence of severe regurgitation. The purpose of this study was to explore the basic determinants of PV inflow in the presence and absence of regurgitation. In particular, the hypothesis that systolic PV flow depends on the interaction of regurgitant volume with atrial and PV properties (compliance, initial volume, total area of the pulmonary veins at the atrial junction, and the inertia of PV inflow) was tested and further, that the combination of these variables, rather than regurgitant volume alone, determines PV inflow. A mathematical model of the atrium and pulmonary veins was developed. Atrial and PV pressure were modeled as the product of chamber elastance and volume, where atrial elastance varied in time to simulate atrial relaxation and descent of the mitral anulus. A simplification of the modified unsteady Bernoulli equation was used to compute the PV velocities that resulted from the developed pressure gradient. The modeling was performed over a range of initial atrial elastances (0.77 to 0.2 mm Hg/cc), initial atrial volumes (20 to 75 cc), total PV areas (3.12 to 5.12 cm2), and PV inflow inertances (8 to 18 gm/cm2), with and without the addition of two regurgitant jets (regurgitant volume of 20 and 60 cc). The model realistically simulated the systolic PV waveform in magnitude and morphology. As the volume of regurgitation increased, PV peak flow velocity decreased, and eventually late systolic flow reversal occurred. However, the peak flow velocity, the time to peak flow, and the presence and magnitude of flow reversal were influenced by atrial compliance, volume, total atrial inlet area, and PV inflow inertia. This study found that PV flow blunting and reversal increased as atrial compliance, volume, and PV inertia decreased and as atrial inlet area increased. Atrial and PV properties (compliance, volume, total PV atrial inlet area, and PV inflow inertia), acting in combination, mediate the physiologic impact of the regurgitant lesion in terms of the resulting rise in atrial pressure as reflected by the pattern of systolic PV influx. For example, PV flow reversal is more likely in acute compared with chronic regurgitation because the atrium is less compliant and has a smaller initial volume. Therefore, the clinical assessment of mitral regurgitation using changes in systolic PV flow must be viewed in the context of atrial and PV properties.

Acceleration↗
PubMed1997

Mid-systolic drop in left ventricular ejection velocity in obstructive hypertrophic cardiomyopathy--the lobster claw abnormality.

UNLABELLED: In many patients with obstructive hypertrophic cardiomyopathy, an abrupt mid-systolic drop in left ventricular ejection velocity can be detected. We analyzed 27 patients with obstructive hypertrophic cardiomyopathy who had 43 echocardiographic examinations (mean gradient 53 +/- 6 mm Hg). Exams showing a mid-systolic drop had higher mean outflow tract pressure gradients (90 +/- 6 compared with 29 +/- 4 mm Hg, p < 0.001). After medical elimination of obstruction, the mid-systolic drop was no longer seen. We measured 105 pulsed-wave Doppler tracings in the left ventricular cavity and compared them with 90 continuous-wave tracings through the outflow tract. There was a close temporal correlation between the nadir of the left ventricular velocity drop and the peak continuous-wave left ventricular outflow tract velocity (r = 0.99). There was also a close temporal correlation between the onset of the fall in pulsed velocity and the onset of M-mode mitral-septal contact (r = 0.95). CONCLUSIONS: The mid-systolic drop in left ventricular velocity is due to impedance to ejection and provides evidence of true obstruction. As left ventricular ejection velocity falls to its mid-systolic nadir because of impedance of ejection, velocity downstream in the left ventricular outflow tract actually rises to its peak. This disparity in the two velocities, deceleration in the left ventricular cavity and acceleration in the left ventricular outflow tract, indicates that the outflow orifice is progressively narrowed over time as the mitral valve is forced into the septum by the rising pressure difference. The obstruction phase is best described as a time-dependent, amplifying feedback loop. The orifice narrows over time because of the rising pressure difference; the pressure difference rises over time because of the narrowing orifice.

Acceleration↗
PubMed1998

Effect of dobutamine stress on left ventricular systolic and diastolic functions in patients with moderate to severe left ventricular dysfunction.

Dobutamine stress echocardiography (DSE) is increasingly used in patients with moderate and severe left ventricular (LV) dysfunction. However, its effect on central and peripheral hemodynamics and LV function in this patient population is not known. This study investigates the effect of dobutamine stress on LV systolic and diastolic performance and peripheral hemodynamics in 177 consecutive patients undergoing DSE. Sixty-five patients with an LV ejection fraction (EF) of < or =40% were compared with 112 patients with an EF of >40%. Compared with those with EF > 40%, patients with EF < or =40% had a faster heart rate(76 +/- 13 vs 70 +/- 13 bpm, p < 0.001), lower systolic blood pressure (127 +/- 18 vs 133 +/- 20 mm Hg, p < 0.05), lower stroke volume (60 +/- 20 vs 74 +/- 36, p = 0.01), longer LV isovolumic relaxation time (118 +/- 37 vs 108 +/- 25 msec, p < 0.05) and larger LV end-diastolic (57 +/- 9.6 vs 49 +/- 7 mm, p < 0.0001) and end-systolic (46 +/- 10 vs 32 +/- 7.9 mm, p < 0.0001) diameters. They also had a lesser increment in cardiac output (1.5 +/- 1.6 vs 3.2 +/- 4.8 L/min, p = 0.02), a smaller reduction of systolic LV size (-5.3 +/- 4.1 vs -7.0 +/- 4.3 mm, p < 0.05) and a lower propensity to LV cavity obliteration with dobutamine infusion. In conclusion, patients with an EF < or =40% have lower baseline stroke volume, systolic blood pressure, higher heart rate, and longer LV isovolumic relaxation time. They also have a smaller increase in cardiac output, a smaller reduction of LV size, and a lower propensity to LV cavity obliteration with dobutamine stress.

Adrenergic beta-Agonists↗
PubMed1999

Left ventricular systolic wall motion velocities along the long and short axes measured by pulsed tissue Doppler imaging in patients with atrial fibrillation.

Pulsed tissue Doppler imaging was performed to measure systolic left ventricular (LV) posterior wall motion velocity along the long and short axes and to evaluate the relationships between the systolic variables and the maximum first derivative (peak dP/dt) of the LV pressure curve and the 2 preceding R-R intervals in 39 patients with atrial fibrillation (AF). The study group consisted of 22 patients with AF only, 17 patients with dilated or ischemic cardiomyopathy and AF, and 25 healthy control subjects in sinus rhythm. The systolic component of the LV posterior wall motion velocity was divided into the first (Sw1) and second (Sw2 ) systolic waves. The peak Sw1 along the long axis was greater than either that along the short axis or the peak Sw2s along the long and short axes in the control and AF-only groups. The peak Sw1 along the long axis was lower in the AF-only group than in the control group, and those along the short and long axes were lower in the dilated AF group than in the other groups. The peak Sw1 almost coincided with the peak dP/dt. The peak Sw1 along the long axis correlated closely with the peak dP/dt, and the ratio of the preceding R-R interval to the interval before the preceding ("prepreceding") R-R interval in both AF groups, particularly in the dilated AF group, and the slopes of their relationships were steeper in the dilated AF group than in the AF-only group. The peak Sw2 along the short axis was greater than that along the long axis in the control and AF-only groups. The peak Sw2 along the long axis was lower in the AF-only group than in the control group, and those along the short and long axes were lower in the dilated AF group than in the other groups. The peak dP/dt was lower and the LV end-diastolic pressure was higher in the dilated AF group than in the other groups. In conclusion, peak Sw1 along the long axis is useful for the evaluation of isovolumic myocardial LV contractility, and the interval-force relation and the Frank-Starling mechanism are important factors of beat-to-beat variability in systolic LV function in patients with AF.

Atrial Fibrillation↗
PubMed2001

Systolic blood pressure alterations during hyperinsulinemia are related to changes in ionized calcium status.

BACKGROUND: A correlation between changes in ionized calcium status and changes in systolic blood pressure (BP) has previously been observed during induced euglycemic hyperinsulinemia in patients with essential hypertension. The objective of this study was to evaluate associations between alterations in ion status and BP changes during euglycemic hyperinsulinemia in healthy normotensive subjects. METHODS: Ion status in plasma and BP were measured before and at the end of euglycemic hyperinsulinemic clamp tests performed in 41 healthy normotensive volunteers. RESULTS: During euglycemic hyperinsulinemia plasma sodium increased by 1% (P < .0001), ionized calcium (iCa) by 5% (P < .0001), and ionized magnesium (iMg) by 4% (P < .01), whereas potassium decreased by 10% (P < .0001). The changes in plasma iCa and iMg correlated significantly to changes in systolic BP (r = -0.38, P < .02; r = -0.32, P < .05, respectively), but the correlation between changes in iMg and changes in systolic BP did not remain significant in a multiple regression model. The glucose infusion rate correlated inversely to the change in iMg (r = -0.39, P < .01). CONCLUSIONS: The group mean systolic BP was unaltered during induced euglycemic hyperinsulinemia in healthy normotensive subjects; however, a more pronounced increase in the circulating iCa concentration was associated with a greater decline in systolic BP, which is in accordance with previous observations in patients with essential hypertension. The group mean diastolic BP was decreased; however, the lowered diastolic BP was not correlated to changes in ion status.

Adult↗
PubMed1997

Is diastolic hypertension an independent risk factor for stroke in the presence of normal systolic blood pressure in the middle-aged and elderly?

In a prospective population-based study from the Copenhagen City Heart Study, the role of diastolic blood pressure as an independent risk factor of stroke, in the presence of normal systolic blood pressure, was assessed in 6,545 subjects aged 50 to 80 years. Follow-up was 12 years. Subjects were divided into various blood pressure categories according to both diastolic and systolic blood pressure. The risk of stroke was assessed using a multivariate Cox proportional hazards model, taking into account various cardiovascular risk factors (age, sex, smoking, diabetes mellitus, body mass index, and levels of serum cholesterol). After adjustment for risk factors, only subjects with elevated systolic blood pressure had a significantly increased risk of future stroke. The risk of stroke according to blood pressure categories further reflected increasing levels of pulse pressure, with the highest risk of stroke in subjects with the greatest pulse pressure. We conclude that systolic blood pressure is a better predictor of stroke than is diastolic blood pressure, and question whether diastolic blood pressure, in the presence of normal systolic blood pressure, is an independent risk factor for stroke in the middle-aged and elderly.

Age Factors↗
PubMed1999

Modified ultrafiltration improves global left ventricular systolic function after open-heart surgery in infants and children.

OBJECTIVES: Modified ultrafiltration increases blood pressure and cardiac index following open-heart surgery in children, but it is unclear if this is secondary to an improvement in global left ventricular function. A previous report has suggested that left ventricular systolic function as assessed in a single chord is improved by ultrafiltration (Davies MJ, Nguyen K, Gaynor JW, Elliott MJ. Modified ultrafiltration improves left ventricular systolic function in infants after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1998;115:361--370). The prominent vascular actions of modified ultrafiltration necessitate left ventricular assessment using load-independent indices of systolic and diastolic function. METHODS: In 22 consecutive infants and children undergoing open-heart surgery, left ventricular function was assessed following bypass and then 10 min later. Sixteen children (median weight 8.1 kg) underwent modified ultrafiltration during this period, the remainder (median weight 7.3 kg) were controls for spontaneous recovery without ultrafiltration. Real-time pressure-volume loops, with transient inferior caval vein snaring were generated from conductance and microtip pressure catheters inserted through the LV apex. From these, load-independent (slope of the end-systolic pressure-volume [Ees] and end-diastolic pressure-volume [Eed] relationships) and load-dependent (Pmax, maximum LV pressure; Ped, end-diastolic LV pressure; maximum [dP/dtmax] and minimum [dP/dtmax] time derivatives of LV pressure; tau, time constant of isovolumic relaxation) indices of left ventricular function were measured. RESULTS: Haemoconcentration was achieved in all modified ultrafiltration patients, median increase in haematocrit 34% (interquartile range 21%, 42%), final haematocrit 0.40 (0.35, 0.41). Ees increased 58% (9, 159, P = 0.005). The changes in Eed, Pmax, Ped, dP/dtmax, dP/dtmin, and tau were not significantly different from the control group. CONCLUSION: Modified ultrafiltration improves global left ventricular systolic function in infants and children following open-heart surgery.

Cardiac Surgical Procedures↗
PubMed2002

Intermediate effects of treatment with metoprolol or carvedilol in children with left ventricular systolic dysfunction.

The use of beta-blocking agents in adults with congestive heart failure has been shown to improve symptoms and outcome; however, experience in pediatric patients with left ventricular systolic dysfunction is limited. We identified 12 pediatric patients treated with beta-blocking agents for left ventricular systolic dysfunction and reviewed echocardiographic indices of left ventricular systolic performance prior to initiation of beta-blocker therapy and at intermediate follow-up. Left ventricular fractional shortening and ejection fraction increased significantly from baseline to intermediate follow-up (13 +/- 4% to 21 +/- 8% [p = 0.01] and 26 +/- 8% to 41 +/- 17% [p = 0.04], respectively). When added to conventional therapy, beta-blocker therapy resulted in an increase in ejection-phase indices of left ventricular systolic performance at intermediate follow-up in pediatric patients with systolic dysfunction.

Adolescent↗
PubMed1999

Second by second patterns in cortical electroencephalograph and systolic blood pressure during Cheyne-Stokes.

Little is known about how arousal develops during the ventilatory phase of Cheyne-Stokes breathing. This study employs neural network analysis of electroencephalograms (EEGs) to describe these changes and relate them to changes in systolic blood pressure, which is probably a subcortical marker of arousal. Six patients with Cheyne-Stokes respiration (apnoea/hypopnoea index 32-69 h(-1)) caused by stable chronic heart failure underwent polysomnography including arterial beat-to-beat systolic blood pressure determination. Periods of 15 sequential apnoeas during nonrapid eye movement sleep were identified for each subject. For each apnoea, the EEG was examined second-by-second using neural net analysis from 28 s before to 28 s after apnoea termination (first return of oronasal airflow), and this was compared with the systolic blood pressure pattern. During the apnoeic phase, sleep deepened progressively. Arousal started to develop at or just before apnoea termination and progresses through the breathing phase. The rise and fall in the systolic blood pressure closely followed the rise and fall in electroencephalographic sleep depth. In conclusion, during Cheyne-Stokes breathing, cortical electroencephalographic arousal begins at or just before the resumption of breathing. Cortical electroencephalographic sleep depth changes are closely mirrored by changes in arterial systolic blood pressure, suggesting that the state changes in the cortical and basal brain structures may be synchronous.

Arousal↗