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PubMed2004

Na+/H+ exchange inhibition attenuates left ventricular remodeling and preserves systolic function in pressure-overloaded hearts.

Cardiac hypertrophy is a homeostatic response to elevated afterload. Na+/H+ exchanger (NHE) inhibition reduces the hypertrophic response in animal models of left ventricular hypertrophy (LVH) and myocardial infarction. We examined the effect of chronic treatment with cariporide, a selective inhibitor of Na+/H+ exchanger isoform 1 (NHE-1), on left ventricular (LV) systolic and diastolic function under pressure overload conditions. Male CD-1 mice were randomized to receive either a control diet or an identical diet supplemented with 6000 p.p.m. of cariporide. Cardiac pressure overload was induced by thoracic aortic banding. LV dimension and systolic and diastolic function were assessed in sham and banded mice by echocardiography and cardiac catheterization 2 and 5 weeks after surgery. Histological analysis was also performed. After 2 weeks of pressure overload, the vehicle-treated banded mice (Veh-Bd) had enhanced normalized LV weight (about +50%) and normal chamber size and function, whereas cariporide-treated banded mice (Car-Bd) showed a preserved contractility and systolic function despite a marked attenuation of LVH. Diastolic function did not differ significantly among groups. After 5 weeks, the Veh-Bd developed LV chamber enlargement and systolic dysfunction as evidenced by a 16% increase in LV end-diastolic diameter, a 36% decrease in myocardial contractility, and a 26% reduction in percent fractional shortening. In contrast, Car-Bd showed an attenuated increase in LV mass, normal chamber size, and a maintained systolic function. A distinct histological feature was that in banded mice, cariporide attenuated the development of cardiomyocyte hypertrophy but not the attendant myocardial fibrosis. In conclusion, the results of the present study indicate that (i) the hypertrophic response to pressure overload is dependent on NHE-1 activity, and (ii) at the 5-week stage, banding-induced deterioration of LV performance is prevented by NHE-1 inhibition.British Journal of Pharmacology (2004) 141, 526-532. doi:10.1038/sj.bjp.0705631

Animals↗
PubMed1999

Baroreflex sensitivity changes with calcium antagonist therapy in elderly subjects with isolated systolic hypertension.

In order to study the effects of calcium-blocking therapy on cardiovascular homeostasis in elderly subjects with isolated systolic hypertension, we performed a randomised double-blind placebo-controlled crossover study of 6 weeks therapy with modified-release nifedipine or placebo. Changes with calcium-blocker treatment in clinic and 24-h blood pressure (BP), heart rate, BP variability, baroreflex sensitivity (BRS) by three methods (Valsalva manoeuvre, phenylephrine and sodium nitroprusside injection), and in baroreflex- and non-baroreflex-mediated reflexes (tilt and cold face stimulus) were studied in 14 elderly subjects (mean age [+/- SEM] 70 +/- 1 years) with sustained isolated systolic hypertension (clinic BP 179 +/- 3/85 +/- 1 mm Hg). Clinic systolic BP, but not diastolic BP, was reduced with treatment (by 14 +/- 6 mm Hg, P = 0.03, diastolic BP 4 +/- 3 mm Hg, P = 0.16). Twenty-four hour BP was also reduced by nifedipine treatment (by 18 +/- 3/9 +/- 2 mm Hg, both P < 0.001). Clinic and 24-h heart rate, and daytime BP variability, were unchanged with treatment. BRS was significantly increased during nifedipine therapy by all three measurement methods (all P < 0.05). With 60 degrees tilt during active treatment, subjects exhibited a greater heart rate increase (P < 0.01), and a reduced fall in systolic (P < 0.05) and diastolic BP (P < 0.05). Thus despite the arteriosclerosis and reductions in large artery compliance described in elderly patients with isolated systolic hypertension, clinically important improvements in clinic and ambulatory BP and some aspects of cardiovascular homeostasis can be achieved with calcium-channel blocking therapy.

Age Factors↗
PubMed2002

Left ventricular mass and systolic dysfunction in essential hypertension.

A relation between left ventricular (LV) hypertrophy and depressed midwall systolic function has been described in hypertensive subjects. However, a strong confounding factor in this relation is concentric geometry, which is both a powerful determinant of depressed midwall systolic function and a correlate of LV mass in hypertension. To evaluate the independent contribution of LV mass to depressed systolic function, 1827 patients with never-treated essential hypertension (age 48 +/- 12 years, men 58%) underwent M-mode echocardiography under two-dimensional guidance. Relative wall thickness was the strongest determinant of low midwall fractional shortening (r = -0.63, P < 0.0001). The significant inverse relation observed between LV mass and midwall fractional shortening (r = -0.43, P < 0.0001) persisted after taking into account the effect of relative wall thickness (partial r = -0.27, P < 0.0001). Within each sex-specific quintile of relative wall thickness, prevalence of subnormal afterload-corrected midwall systolic function was greater in subjects with, than in subjects without, LV hypertrophy (P < 0.05 for the first, third, fourth and fifth quintile). In a multiple linear regression analysis, both LV mass (P < 0.0001) and relative wall thickness (P < 0.0001) were independent predictors of a reduced midwall fractional shortening. In conclusion, the inverse association between LV mass and midwall systolic function is partly independent from the effect of relative wall thickness. LV hypertrophy is a determinant of subclinical LV dysfunction independently of the concomitant changes in chamber geometry.

Adult↗
PubMed2005

Treatment of systolic hypertension: spotlight on recent studies with angiotensin II antagonists.

Systolic blood pressure has a continuous, graded, strong, independent, and aetiologically significant relationship to mortality from coronary heart disease, stroke, and all cardiovascular diseases, as well as to all-cause mortality and life expectancy. Angiotensin II (AII) may be intimately involved in the pathogenesis of systolic hypertension through multiple mechanisms, including decreasing the elastin content and increasing the collagen content of the arterial wall, thickening and fibrotic remodelling of the vascular intima, and proliferating smooth muscle cells in the arterial wall, resulting in increased thickness, stiffening, and partial loss of contractility. AII antagonists may therefore offer hitherto unrecognized benefits (independent of blood pressure) on age-related vascular damage and provide particular benefits in patients with systolic hypertension. Recent evidence has demonstrated that losartan offers cardiovascular outcomes benefits in isolated systolic hypertension (ISH) associated with an excellent tolerability profile. This, in patients with ISH, AII antagonists more facilitate systolic BP control, providing cardiovascular protection and offering an excellent risk-benefit profile.

Angiotensin II↗
PubMed1996

Ambulatory monitoring of blood pressure disturbs sleep and raises systolic pressure at night in patients suspected of suffering from sleep-disordered breathing.

1. The aim of the study was to assess the effect of ambulatory monitoring of blood pressure on sleep and on blood pressure in middle-aged patients. 2. Nine consecutive patients (seven men, two women; mean age 57 years) complaining of snoring and various degrees of excessive daytime somnolence were studied. Five patients were normotensive and four were being treated for hypertension. During one night standard laboratory polysomnography was performed with monitoring of blood pressure by a silent ambulatory monitor and continuous infrared blood pressure by photoplethysmography. 3. Ambulatory blood pressure significantly disturbs sleep architecture, causing EEG arousals in 64% of measurements, and induces a significant rise in blood pressure during systolic pressure measurement by the ambulatory monitor (rise in systolic pressure, 13.7 +/- 15.9 mmHg, P < 0.001; rise in diastolic pressure, 3.7 +/- 8.2 mmHg, P < 0.01). At the time of diastolic measurement, blood pressure had returned to the preinflation value. The rise in systolic blood pressure was higher when an arousal was associated with cuff inflation (P < 0.001). This rise in blood pressure is probably the consequence of sympathetic nervous system activation. 4. We conclude that ambulatory blood pressure recordings of systolic blood pressure during sleep should be interpreted with caution as systolic blood pressure may be significantly increased in patients suspected of suffering from sleep-disordered breathing.

Adult↗
PubMed2000

Effects of spironolactone on systolic blood pressure in experimental diabetic rats.

BACKGROUND: Mineralocorticoid hormones, which maintain electrolyte balance and blood pressure, are thought to be associated not only with the expression of renal 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), but also with that of intracellular mineralocorticoid receptors (MRs). The present study was designed to test whether the mineralocorticoid action of glucocorticoid corticosterone on renal MR is involved in the development of diabetes-associated hypertension by measuring the alterations of renal 11beta-HSD2. METHOD: We measured the mean systolic blood pressure, renal 11beta-HSD1, and mRNA levels in streptozotocin (STZ)-induced diabetic rats that received spironolactone, insulin, or no treatment, and in nondiabetic controls that received spironolactone. RESULTS: Four weeks after an injection of STZ, the renal 11beta-HSD2 and mRNA levels were significantly lower in diabetic rats than in control rats, and the mean systolic blood pressure was 14.8% higher in diabetic rats than in controls. Subcutaneous injections of spironolactone into diabetic rats for three weeks partially reversed the decrease in renal 11beta-HSD2 activity and gene expression, and prevented the mean systolic blood pressure elevation. Spironolactone treatment for one week also resulted in a significant reduction in mean systolic blood pressure during the development of diabetic hypertension. However, treatment with STZ did not significantly decrease the renal 11beta-HSD1 activity and mRNA expression, and spironolactone treatment did not exert a significant effect on this enzyme in STZ-induced diabetic rats. CONCLUSION: In the development of diabetes-induced hypertension, the effect of spironolactone on mean systolic blood pressure may be associated with the mineralocorticoid effects of corticosterone on renal MR, as well as an alteration of renal 11beta-HSD2 activity and its mRNA expression in insulin-dependent diabetic rats.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2002

Intramyocardial analysis of regional systolic and diastolic function in ischemic heart disease with Doppler tissue imaging: role of the different myocardial layers.

BACKGROUND: Preliminary experimental data have shown a nonuniform distribution of myocardial velocities (MVs) across the myocardial wall in normal conditions. However, after ischemic damage to the myocardium, a different pattern of reduction in the myocardial layers has been reported. The aim of this study is to analyze the spatial distribution of MVs and the resultant myocardial velocity gradients (MVGs) during the systolic and diastolic time periods. Doppler tissue imaging (DTI) in color M-mode was used to evaluate 3 different myocardial layers (endocardium, mesocardium, and epicardium) and their changes as a result of ischemia. METHODS: Thirty-two consecutive patients were studied with DTI color M-mode: 18 patients with a history of previous or ongoing myocardial infarction and 14 healthy subjects. Postprocessing of images was accomplished with proprietary software. MV and MVG values of all layers along both systolic and diastolic time were calculated. For temporal analysis, systole was subdivided in 3 equal periods. Early- and late-diastolic times were also identified. RESULTS: In ischemic patients, the mean MV and maximum MV throughout systole decreased significantly in the endocardium and mesocardium, whereas only slightly in the epicardium. The mean MVG was less in ischemic patients (0.66 +/- 0.11 vs 0.23 +/- 0.15, P <.03). Temporal analysis showed a decrease in the maximal MV and MVG in all layers over the 3 systolic periods. This decrease was the more consistent in mesocardium. In diastole, there was a decrease in maximal MV in all layers, being more pronounced in endocardium and mesocardium. Diastolic mean MVG was shown to be different between control and ischemic groups (-0.2 +/- 0.05 vs -0.10 +/- 0.04, P <.06). A significant decrease of the maximal MV in endocardium and mesocardium was reported in the temporal analysis during early diastole. No change was reported in the epicardium. The MVG value also showed a significant decrease (-2.69 +/- 0.29 vs -1.59 +/- 0.89, P <.02). In ischemic patients in late diastole, the maximum MV was increased in all layers of the myocardium, and this increase was observed mainly in the endocardium. An increase in the MVG (-0.78 +/- 0.18 vs -1.47 +/- 0.85, P = NS) was also reported during late diastole. CONCLUSION: There is a nonuniform distribution of velocities in the different myocardial layers under normal conditions. This distribution of velocities undergoes a significant change in patients with ischemic myocardial damage. Intramyocardial wall motion analysis could have clinical applications in both the early detection of ischemia and myocardial viability.

Adolescent↗
PubMed2003

A comparison between middle cerebral artery peak systolic velocity and amniotic fluid optical density at 450 nm in the prediction of fetal anemia.

OBJECTIVE: The purpose of this study was to compare fetal middle cerebral artery peak systolic velocity with amniotic fluid delta optical density at 450 nm in the prediction of fetal anemia. STUDY DESIGN: A prospective study that involved 28 singleton pregnancies that were at-risk for fetal anemia was carried out in a tertiary teaching hospital. Middle cerebral artery peak systolic velocity was measured immediately before the determination of deltaoptical density at 450 nm and fetal hemoglobin concentration. Sensitivities and predictive values for fetal anemia were examined. RESULTS: Fetal hemoglobin concentrations correlated significantly with middle cerebral artery peak systolic velocity (correlation coefficient, -0.77; P <.0001) and deltaoptical density at 450 nm zones (correlation coefficient, -0.56; P =.0025). Middle cerebral artery peak systolic velocity was >1.5 multiples of the median in 15 of 28 cases (54%); for this cutoff value, the sensitivity and positive-predictive values for a hemoglobin deficit of >-3SD were 75% and 60% and for a hemoglobin deficit of >-5SD were 100% and 47%, respectively. The corresponding values for deltaoptical density at 450-nm zone III (6/28 cases, 21%) were 0% (hemoglobin deficit, <-3SD) and 86% and 100% (hemoglobin deficit, <-5SD). CONCLUSION: Middle cerebral artery peak systolic velocity and amniotic fluid optical density at 450 nm are both useful in the prediction of fetal anemia. However, Doppler examination has the advantage of being a noninvasive method that can help reduce the number of invasive procedures in pregnancies that are at-risk for fetal anemia.

Adult↗
PubMed2002

Isolated systolic hypertension, obesity, and hyperkinetic hemodynamic states in children.

OBJECTIVE: To determine the factors that contribute to the pathogenesis of isolated systolic hypertension in children. METHODS: School-based measurement was performed of blood pressure (BP), heart rate, weight, and height in 2460 students (49% Hispanic, 31% black, 13% white) 12 to 16 years of age in 8 urban public schools. An independent group of 71 untreated children underwent 24-hour ambulatory BP monitoring (ABPM) to confirm clinic hypertension and assess circadian BP patterns. RESULTS: Hypertension and obesity were found in 17% and 23% of students, respectively. Among hypertensive students, 88% (363/413) had isolated systolic hypertension. Hypertension was more prevalent in obese than nonobese students (33% vs 11%, P <.0001). Obese hypertensive students had higher resting heart rate than nonobese normotensive patients (85.9 vs 79.6 beats/min, P <.001). Among patients who underwent ABPM, isolated systolic hypertension was found in 51% (36/71) by clinic BP and in 62% (18/29) with confirmed hypertension by ABPM. Blood pressure variability during daytime and sleep periods was higher in obese than nonobese patients for systolic BP (P <.01) and diastolic BP (P <.05). CONCLUSIONS: The findings of increased heart rate and BP variability in obese children with isolated systolic hypertension suggest that sympathetic nervous system hyperactivity may contribute to its pathogenesis.

Adolescent↗
PubMed1989

Systolic hypertension in the elderly. Relationship with cardiovascular disease.

The risk of stroke and myocardial infarction is increased in patients with elevated systolic blood pressure. Although treatment trials have demonstrated the benefit of antihypertensive therapy in elderly patients with diastolic hypertension, the only trial conducted in elderly patients with isolated systolic hypertension is currently in progress. A six-month trial of nonpharmacologic therapy should generally be the initial treatment in patients with isolated systolic hypertension. Then, if systolic pressure remains elevated, a cautious trial of drug treatment is reasonable. The drug used should be started in a low dose, and the dose should be titrated slowly. With this approach, antihypertensive treatment of elderly patients with isolated systolic hypertension may be well tolerated and ultimately beneficial.

Aged↗
PubMed2000

The placebo effect and white coat effect in isolated systolic hypertension and systo-diastolic hypertension.

It is well recognised from many clinical trials that there is a blood pressure lowering effect when placebo is administered to patients with essential hypertension ("placebo effect"). The reduction in blood pressure, however, may also be partly due to loss of the alerting response ("white coat effect") as a result of familiarisation with the clinical environment. To investigate the hypothesis that there may be a more marked placebo effect and white coat effect in isolated systolic hypertension (ISH) compared with systo-diastolic hypertension (SDH), we studied 78 patients with hypertension: 34 had ISH and 44 patients had SDH. The 34 patients with ISH were older (68.7 vs 54.9 years), had a higher SBP (192.2 vs 169.6 mmHfg) and lower DBP (85.5 vs 102.0 mmHg) when compared to patients with SDH. Amongst the patients with ISH, there were no significant changes in mean blood pressures pre-placebo (paired t-test, p = NS). In the placebo period, there was a significant reduction in systolic blood pressures at all three points, and a significant reduction in diastolic blood pressures after 2 and 3 months placebo (paired t-test, p < 0.05). There was a mean reduction in mean systolic blood pressure at visit 1 by 5.2%, visit 2 by 5.1% and visit 3 by 4.6%, when compared to mean pre-placebo systolic blood pressures (p < 0.05). The mean reduction in diastolic blood pressure was 5.8% at visit 2 and 3.5% at visit 3, when compared to mean pre-placebo diastolic blood pressure (p < 0.05). At the 4-week visit after receiving placebo, the mean systolic blood pressure decreased by 9.4 mmHg (p = 0.003) and mean diastolic blood pressure by 2.7 mmHg (p = NS) in the patients with ISH. In patients with SDH, there were no statistically significant changes in recorded BP readings following the introduction of placebo. We suggest blood pressures in some patients with ISH may settle with careful follow up and initiation of treatment in these patients could potentially be delayed for at least 3 months, as therapy may not prove necessary.

Adult↗
PubMed2004

Left ventricular ejection fraction calculation from automatically selected and processed diastolic and systolic frames in short-axis cine-MRI.

The calculation of the left ventricular ejection fraction (LVEF) is dependent upon the accurate measurement of diastolic and systolic left ventricular volumes. Although breath-hold cine magnetic resonance imaging (MRI) allows coverage of the whole cardiac cycle with an excellent time resolution, many authors rely on the visual selection of diastolic and the systolic short-axis slices in order to reduce the postprocessing time. An automatic method was developed to detect the endocardial contour on each image, allowing an automatic selection of the systolic frame. The calculated ejection fraction was compared with radionuclide ventriculography (RNV). Sixty-five patients were examined using an electrocardiogram (ECG)-gated gradient echo sequence. Among these examinations, manual and automatic processing with MRI were compared when the time of the systolic frame concorded. Good correlations have been found between the automatic MRI approach and RNV, and between manual and automatic processing on MRI alone. The results show that the automatic determination of the ejection fraction is feasible, and should constitute an important step toward a larger acceptance of MRI as a routine tool in heart disease imaging. One major benefit of using automatic postprocessing is that it may eliminate the visual choice of the systolic frame, inaccurate in more than 50% of the studied patients.

Adult↗
PubMed1985

End-systolic pressure-volume relations of isolated ejecting rabbit left ventricles after quick diastolic volume changes.

The aim of the study was to investigate the influence of quick diastolic volume changes on systolic performance of ejecting left ventricles. To measure left ventricular systolic performance the maximum ratio of ventricular pressure (P) and volume (V) was calculated on beat-to-beat basis when the diastolic loading conditions were varied in different ways. These end-systolic P-V (P-VES) points were obtained from both isovolumic and ejecting contractions. A deviation from the P-VES relation is thought to result from factors changing the inotropic condition of the heart. When steady state isovolumic and ejecting P-VES data were collected linear P-VES relations were found. The relations coincided when stroke volumes were not too large. When the diastolic volume was quickly changed (ie 10 to 20 ms) late in diastole, the P-VES points of the resulting contractions showed a significant deviation from the steady state relation (p less than 0.001). This deviation was dependent on the magnitude of the volume step. After quick volume infusions the heart ejected to end-systolic volume (ESV) values that were smaller than expected from the steady state P-VES relation and the end-systolic pressure (ESP) was larger. After quick volume withdrawals ESV values were larger and ESP was smaller than expected. The magnitude of the effect was not dependent on the preset basic diastolic volume if the volume changes were considered as fractions end-diastolic volumes (EDV). It is concluded that when diastolic volumes are varied just before stimulation, a significant deviation of the P-VES point from the steady state P-VES relation is found in the following contraction. This phenomenon suggests an alteration in the inotropic state of the heart.

Animals↗
PubMed1988

Left ventricular systolic series elastic properties in aortic stenosis before and after valve replacement.

In seven patients with aortic valve disease the time course of an auxotonic beat was compared with that of an isovolumetric beat produced by aortic cross clamping during open heart surgery. The rate of systolic stress rise (dS/dt; g.cm-2) of the isovolumetric beat at peak meridional wall stress (Sp; g.cm-2) of the auxotonic beat was determined by tipmanometry and simultaneous sonomicrometry and was found to be 87% of maximum dS/dt. In the second part of the study the stiffness index (k) was calculated in patients undergoing cardiac catheterisation according to: k = 0.87.(max.dS/dt)/Sp.Vcf, where Vcf = normalised midwall circumferential fibre shortening velocity (circ.s-1). In 22 patients, 10 controls and 12 patients with aortic stenosis before (pre) and after (post) valve replacement the systolic stiffness index k (circ-1) was determined using tipmanometry and frame by frame angiocardiography. Muscle fibre diameter and interstitial fibrosis were assessed from left ventricular endomyocardial biopsies. The systolic stiffness index k was 15 circ-1 in controls, 14 in preoperative patients with aortic stenosis and 12 (p less than 0.01 v controls) in postoperative patients. There was a significant correlation between k and muscle fibre diameter (r = 0.55; p less than 0.01) but not between k and interstitial fibrosis or ejection fraction. We conclude that systolic stiffness index k is normal despite marked left ventricular hypertrophy in preoperative patients with aortic stenosis. Following successful valve replacement systolic stiffness index decreased and was significantly lower than in controls. Series elasticity appears to be determined by structures related to the muscle cell rather than to interstitial fibrosis.

Aortic Valve Stenosis↗
PubMed1990

Systolic thickening increases from subepicardium to subendocardium.

STUDY OBJECTIVE: The aim was to determine the relation between systolic function and depth below the epicardial surface, using pulsed Doppler crystals. DESIGN: Systolic excursion in mm was measured at multiple depths below the epicardial surface. Measurements were made during control conditions. SUBJECTS: Thirty four anaesthetised mongrel dogs were studied. MEASUREMENTS AND MAIN RESULTS: A total of 333 measurements of systolic excursion were made during control conditions at 1 to 3 crystal sites per dog. Two models were constructed; the model which assumed a quadratic relation between depth (d) and systolic excursion (EX) (EX = 0.498 + 0.176d + 0.006d2) fit the data better than did a model which assumed a linear relation (EX = -0.0716 + 0.254d). CONCLUSIONS: These data support the prediction from geometric models that systolic excursion increases in a non-linear fashion from subepicardium to subendocardium.

Animals↗
PubMed1992

Effects of progressive myocardial ischaemia on systolic function, diastolic dysfunction, and load dependent relaxation.

OBJECTIVE: The aims were to determine (1) the relationship between changes in contractile function (systolic shortening) and the appearance of diastolic dysfunction (postsystolic shortening) during progressive regional left ventricular ischaemia; (2) the effects of increased afterload (acute constriction of the descending thoracic aorta) on ischaemic contractile dysfunction; and (3) the effects of loading during ischaemia on load dependent relaxation. METHODS: Regional myocardial function, using sonomicrometry, was measured in the short and long axes of the apex of the left ventricle of eight open chest anaesthetised dogs (16-20 kg). Progressive apical ischaemia was induced by graded reductions in left anterior descending coronary artery flow (critical constriction, ischaemia 1, ischaemia 2, total coronary occlusion, and postocclusive maximum reactive hyperaemia). Acute afterloading was induced by a snare placed around the descending aorta. RESULTS: Consistent decreases in systolic shortening and increases in postsystolic shortening relative to the total segmental shortening in the short axis of the apical region were seen with worsening ischaemia. Aortic constriction increased the magnitude of apical postsystolic shortening and decreased apical systolic shortening in the short axis during critical constriction, ischaemia 1, and ischaemia 2. Long axis function changed in a qualitatively similar but quantitatively different manner. There was a significant decrease in the load dependency of relaxation with total coronary occlusion. CONCLUSIONS: (1) Changes in systolic and diastolic function occurred concomitantly as mild regional myocardial ischaemia developed and intensified; (2) afterloading significantly worsened regional systolic and diastolic dysfunction during mild ischaemia; and (3) progression of regional ischaemia resulted in loss of load dependent relaxation.

Animals↗
PubMed1994

Coronary perfusion related changes in myocardial contractile force and systolic ventricular stiffness.

OBJECTIVE: The mechanism by which changes in coronary perfusion alter myocardial oxygen consumption (MVO2; Gregg phenomenon) is controversial. This study examined the effect of coronary perfusion on myocardial contractile force and systolic ventricular stiffness in the intact, ejecting heart. METHODS: During selective perfusion of the left anterior descending coronary artery, coronary blood flow was changed with or without concurrent changes in coronary perfusion pressure in 19 alpha chloralose anaesthetised dogs. Regional myocardial segment length (end diastolic length; end systolic length) and developed force were measured with piezoelectric crystals and with a miniature force transducer, respectively. MVO2 was calculated from coronary flow and arteriovenous O2 difference. The slope of the force-length curve during ejection period (delta F/delta SL) was used as an index of systolic myocardial stiffness. RESULTS: When coronary perfusion pressure was varied from 60 to 180 mm Hg (protocol 1, n = 11), maximum developed force (Fmax), delta F/delta SL, and MVO2 increased with perfusion pressure while end diastolic length, segmental shortening, and other haemodynamic variables stayed constant. When coronary blood flow was increased at constant perfusion pressure by infusion of either a low dose or a high dose adenosine (protocol 2, n = 8), Fmax, delta F/delta SL, and MVO2 increased while end diastolic length, segmental shortening, and other haemodynamic variables stayed constant. MVO2 and delta F/delta SL increased more steeply with flow in protocol 1. CONCLUSIONS: (1) Increased coronary blood flow enhances myocardial contractile force, systolic ventricular stiffness, and MVO2 in the intact, ejecting heart. (2) Coronary blood flow induced changes in myocardial contractile force and systolic ventricular stiffness, but not end diastolic length, are probably responsible for coronary blood flow related changes in MVO2.

Adenosine↗
PubMed1993

Discrepancy between systolic and diastolic dysfunction of the left ventricle in patients with Duchenne muscular dystrophy.

To assess the systolic and diastolic dysfunction of the left ventricle (LV) in relation to age and the severity of impairment in Duchenne muscular dystrophy (DMD), we performed M-mode, two-dimensional and pulsed-wave Doppler echocardiography in 45 male subjects with DMD aged 8 to 25 years and in 40 age-matched healthy controls. Systolic dysfunction started in the first decade of life, with some patients showing severe systolic dysfunction in their early teens. This dysfunction, however, did not always depend on the severity of the skeletal muscle disease. No patients with DMD showed an increase in peak atrial velocity and time-velocity integrals of the atrial contraction velocity curve, findings frequently reported to precede the abnormalities in many cardiac diseases; it was thought therefore that these patients had no increase in left atrial compensation. Diastolic dysfunction may not routinely precede or accompany the systolic dysfunction in DMD, in contrast with what is reported in patients with ischaemic or hypertensive heart disease. DMD patients usually show a predominant systolic dysfunction.

Adolescent↗