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PubMed2005

Systolic and diastolic heart failure are associated with different plasma levels of B-type natriuretic peptide.

Previous studies have found that plasma B-type natriuretic peptide (BNP) is elevated during left ventricular systolic or diastolic dysfunction. It is unclear whether the ventricular systolic and diastolic function is associated with different levels of plasma BNP. Plasma BNP was measured in 149 heart failure patients by a rapid point-of-care assay. The patients were divided into left ventricular diastolic dysfunction (n = 48), left ventricular systolic dysfunction (n = 62) and right ventricular systolic dysfunction group (n = 39). The mean BNP level in the left ventricular diastolic dysfunction, left ventricular systolic dysfunction and right ventricular systolic dysfunction was 115 +/- 80 pg/ml, 516 +/- 445 pg/ml and 345 +/- 184 pg/ml, respectively (p < 0.05). We concluded that ventricular systolic and diastolic dysfunction increases plasma BNP levels to a different extent. Left and right ventricular systolic dysfunction is associated with a higher level of plasma BNP than left ventricular diastolic dysfunction.

Adult↗
PubMed2004

Right ventricular long-axis function in relation to left ventricular systolic function.

A decrease in left ventricular (LV) systolic function is accompanied by a decrease in maximal relaxation velocity in LV long-axis direction, but is it also accompanied by a decrease in right ventricular (RV) long-axis function? To study this 35 consecutive patients were examined by echocardiography. Ejection fraction (LVEF) and mitral annulus motion (MAM) were used as indices of LV systolic function and tricuspid annulus motion (TAM), that is the systolic shortening in RV long-axis direction, was used as an index of RV systolic long-axis function. In the same way the maximal relaxation velocity in LV long-axis direction, that is the maximal diastolic velocity of MAM (MDV MAM), has been suggested as an index of LV diastolic function the maximal diastolic velocity of TAM (MDV TAM) can be supposed to be an index of RV diastolic function measuring the maximal relaxation velocity in the RV long-axis direction. A significant positive correlation was found between MDV TAM and MAM (r = 0.64, P<0001) and LVEF (r = 0.54, P = 0.001) and between TAM and the two studied indices of LV systolic function, with the highest correlation to MAM (r = 0.68, P<0.001) and the lowest to LVEF (r = 0.57, P<0.001). Thus, a decrease in LV systolic function is accompanied by a decrease in both systolic and diastolic RV long-axis function, findings that probably are due to the close anatomical connection between the ventricles and to changes that occur in afterload of the RV secondary to LV systolic dysfunction.

Aged↗
PubMed1999

A U-shaped association between home systolic blood pressure and four-year mortality in community-dwelling older men.

BACKGROUND: Several studies in older people have found a U-shaped or J-shaped association of blood pressure with mortality. The increased mortality associated with the lowest levels of blood pressure in older people have been explained by concurrent illnesses and frailty, but previous studies used blood pressure measured on a single occasion. Such a casual value is different from the long-term average of blood pressure. We investigated the relation between the average level of 5-day consecutive home blood pressure and mortality in older people while adjusting for potential confounding factors including morbidity and frailty at baseline. METHODS: In 1992, 1186 community residents of a rural Japanese town, Kahoku, aged 65 or older, measured their blood pressure in their homes 20 times (four times per day, 5 consecutive days). The mean value of the 20 measurements was used to examine the association between home BP and subsequent 4-year mortality. A proportional hazards model was fitted while adjusting for activities of daily living impairment, medical history, antihypertensive medication, smoking, use of alcohol, and depression. RESULTS: A total of 134 persons died during the four-year follow-up period. There was no significant evidence that frailty is more prevalent in the lowest or highest systolic BP group than in intermediate groups. A U-shaped association between the average level of home systolic blood pressure and mortality was found in men while adjusting for potential confounding factors, including morbidity and frailty. We also showed the U-shaped curve of the association of systolic BP with all cause and noncardiovascular mortality in the whole population and the linear association of systolic BP with cardiovascular mortality. CONCLUSIONS: We showed a U-shaped association between the average level of systolic blood pressure measured at home and mortality in older men while adjusting for potential confounding factors including morbidity and frailty. Not only high home systolic BP, but also low home systolic BP, is an independent risk factor for mortality in older men. The mechanisms underlying the association between BP and mortality differ by levels of systolic BP. Cardiovascular deaths tended to be higher in the highest SBP group, and only noncardiovascular deaths were increased in the lowest SBP group. The latter finding suggests that low SBP may be not only an independent risk of mortality but also an indicator of a subclinical noncardiovascular comorbid condition.

Activities of Daily Living↗
PubMed1994

The influence of myocardial systolic shortening on action potential duration following changes in left ventricular end-diastolic pressure.

INTRODUCTION: Contraction-excitation feedback may be an important factor in arrhythmogenesis in patients with heart failure. We have previously demonstrated the contrasting effects of raising left ventricular end-diastolic pressure on action potential duration in dog and guinea pig hearts. The current study was undertaken to assess whether these differing effects might reflect differences in the effect of varying left ventricular end-diastolic pressure on systolic shortening in the two models. METHODS AND RESULTS: Two models were studied and compared. In open chest dog hearts and isolated guinea pig hearts, measurements of myocardial segment length were made while left ventricular end-diastolic pressure was raised and lowered at constant left ventricular peak systolic pressure. Action potentials were also recorded while left ventricular end-diastolic pressure was changed. The dog hearts were studied further in a manner aimed at reproducing the contraction pattern of the guinea pig hearts. In the in situ dog heart, elevation of left ventricular end-diastolic pressure, and the consequent increase in end-diastolic segment length, was accompanied by a marked increase in systolic shortening, such that minimum systolic segment length remained unchanged. Elevation of left ventricular end-diastolic pressure was accompanied by a prolongation of action potential duration. In the in vitro guinea pig model, elevation of left ventricular end-diastolic pressure was accompanied by more modest changes in systolic shortening, which were not sufficient to compensate for increased diastolic segment length. Consequently, minimum systolic segment length increased as the hearts dilated. Elevation of left ventricular end-diastolic pressure was accompanied by a shortening of action potential duration. In a further series of experiments, the effects of increased left ventricular end-diastolic pressure were studied in the dog model while allowing aortic pressure to rise, thereby restricting systolic shortening. Under these circumstances, the dog model was similar to the guinea pig model, with an increase in left ventricular end-diastolic pressure causing a shortening of action potential duration. CONCLUSION: Our results suggest that the effects of preload changes on action potential duration depend on accompanying changes in systolic shortening. This suggests a possible role for contraction-excitation feedback in arrhythmogenesis in patients with regional wall-motion abnormalities.

Action Potentials↗
PubMed1990

A mechanism for the effects of caffeine on Ca2+ release during diastole and systole in isolated rat ventricular myocytes.

1. The fluorescent indicator Indo-1 was used to measure both [Ca2+]i and [caffeine]i in single ventricular myocytes. 2. Caffeine (at concentrations of 1 mM or above) produced a transient increase of resting [Ca2+]i attributed to the release of Ca2+ ions from the sarcoplasmic reticulum (SR). Simultaneous measurement of [caffeine]i showed that the Ca2+ release only began when [caffeine]i had risen to about 1 mM. Subsequently the rate of release was a steep function of [caffeine]i. It is suggested that this results from a positive feedback as the Ca2+ released activates further release. 3. If external Ca2+ was removed the release of Ca2+ produced by caffeine was delayed such that [caffeine]i rose to a greater concentration before release was initiated. This suggests that an increase of [Ca2+]i increases the efficacy of caffeine to release Ca2+ ions from the SR. 4. Lower concentrations of caffeine (50-500 microM) had no effect on diastolic [Ca2+]i. In contrast they increased systolic [Ca2+]i and contraction. This increase was most obvious if the systolic contraction had previously been decreased either by reducing [Ca2+]o from 1 to 0.25 mM or (in voltage-clamped cells) by decreasing the magnitude of the depolarizing pulse. 5. If the exposure to caffeine was prolonged, this increase of systolic [Ca2+]i and contraction was completely transient. On removal of caffeine, systolic [Ca2+]i and contraction decreased to below control before recovering. 6. During these transient changes of systolic [Ca2+]i and contraction there was no change of the sarcolemmal Ca2+ current. 7. It is suggested that the increase of systolic [Ca2+]i is due to caffeine increasing the fraction of the SR Ca2+ content released during the twitch. 8. The above results concerning both diastolic and systolic [Ca2+]i can be explained by a model in which caffeine increases the affinity with which Ca2+ ions activate Ca2(+)-induced Ca2+ release. At high enough [caffeine], the threshold [Ca2+]i for regenerative Ca2(+)-induced Ca2+ release will be reduced to below the resting [Ca2+]i thus producing a diastolic increase of [Ca2+]i. At lower [caffeine] the threshold is higher than resting [Ca2+]i and caffeine only serves to enhance the release produced during systole.

Action Potentials↗
PubMed2000

Effect of verapamil on systolic and diastolic coronary blood flow velocity in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy.

OBJECTIVE: To assess non-invasively the effect of verapamil treatment on coronary blood flow velocity in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy. DESIGN: High frequency transthoracic Doppler echocardiography was used to compare resting phasic coronary blood flow velocity before and after a one month period of verapamil treatment in 17 patients (14 men and three women) with non-obstructive hypertrophic cardiomyopathy. Eighteen healthy subjects formed an age and sex matched control group. Systolic and diastolic coronary blood flow velocity was measured in the distal portion of left anterior descending coronary artery using high frequency transthoracic Doppler echocardiography. Blood flow velocity before and after verapamil was compared in the patients with cardiomyopathy and with the results in the control group. RESULTS: Compared with the controls, patients with hypertrophic cardiomyopathy had increased diastolic coronary blood flow velocity (41.8 (8.1) v 59.9 (21.9) cm/s, p < 0.01) and a lower mean systolic coronary blood flow velocity (18.7 (10.8) v -11.2 (27.5) cm/s, p < 0. 01) before verapamil treatment. A backward pattern of systolic flow, manifested by negative values of coronary blood flow velocity, was recorded in eight of the patients, while no negative values were found in the controls. After verapamil treatment the retrograde systolic blood flow was restored to an anterograde pattern in only one patient. The mean value of systolic coronary blood flow velocity did not change significantly and remained lower than the systolic forward flow velocity in the controls (-3.6 (31.8) v 18.7 (10.8) cm/s, p < 0.05). However, diastolic coronary blood flow velocity decreased significantly after verapamil (59.9 (21.9) v 50.7 (19.5) cm/s p < 0.05), reaching a level comparable with that in the controls (50.7 (19.5) v 41.8 (8.1) cm/s, p > 0.05). CONCLUSIONS: In contrast to healthy subjects, in non-obstructive hypertrophic cardiomyopathy the systolic pattern of coronary blood flow was heterogeneous (both retrograde and anterograde), and diastolic coronary blood flow velocity was abnormally increased, despite a lack of significant symptoms. Verapamil treatment did not restore the forward pattern of systolic blood flow but decreased diastolic blood flow velocity to a level comparable with that in healthy subjects.

Adult↗
PubMed1982

Systolic closure of aortic valve in patients with prosthetic mitral valves.

Systolic closure of the aortic valve was found in 10 of 36 patients who underwent mitral valve replacement. Eight patients had early systolic closure, and two had mid-systolic closure. The left ventricular outflow tract dimension on M-mode and two dimensional echocardiograms, left ventricular posterior wall and septal thickness, left ventricular dimensions in systole and diastole, aortic valve opening, and mitral to aortic valve distance were not significantly different between patients with and without systolic closure of the aortic valve. Two of the 10 patients with systolic aortic valve closure were catheterised and in neither was there a gradient between the left ventricle and the aorta. The two patients with mid-systolic closure, however, were the patients who had the narrowest left ventricular outflow tract which could cause significant distortion of blood flow. Systolic closure of the aortic valve in patients with mitral valve replacement is probably not caused by left ventricular outflow tract obstruction, though abnormalities in laminar flow from the left ventricular outflow tract may be involved.

Adolescent↗
PubMed1983

Mechanism of systolic anterior motion of mitral valve and site of intraventricular pressure gradient in hypertrophic obstructive cardiomyopathy.

The mechanism of systolic anterior motion of the mitral valve and the localisation of the intraventricular pressure gradient were determined in 15 cases of hypertrophic obstructive cardiomyopathy by the combined use of real time two dimensional echocardiography and intracardiac manometry. We arrived at the following conclusions. The systolic anterior motion of the mitral echo in the M-mode echocardiogram can be classified into two types, I and II, based on two dimensional echocardiographic findings. In type I, the echo sources of systolic anterior motion are the anteriorly shifted mitral chordae and, in part, the papillary muscles. The intraventricular pressure gradient occurs at the level of the tip of the papillary muscle. The suprapapillary part of the outflow tract and the inflow part show a low pressure, while the apical cavity shows a high pressure. In type II, the echo sources of systolic anterior motion are the anterior and posterior mitral leaflets which are oriented in such a way as to obstruct the outflow tract. The pressure gradient occurs at the level of the anterior and posterior mitral leaflets. The inflow tract and the outflow tract just below the mitral leaflets show a high pressure, in contrast to type I systolic anterior motion. The inappropriate and maloriented papillary muscles play an essential role in causing both types of systolic anterior motion and outflow obstruction. The direction of the axis of the papillary muscle is changed in late systole, moving its tip away from the interventricular septum, resulting in a simultaneous reduction in systolic anterior motion.

Adult↗
PubMed1984

Influence of dihydralazine induced afterload reduction on systolic time intervals and echocardiography in healthy subjects.

The influence of a pure afterload reduction on systolic time intervals and various echocardiographic indices was assessed in six healthy volunteers, who underwent a single blind placebo controlled trial of three regimens of intravenous dihydralazine (6.25, 12.5, and 25.0 mg). Subsequently autonomic blockade (propranolol and atropine) was used to eliminate the influence of the autonomic reflex action during dosage with dihydralazine 6.25 mg. Dihydralazine increased heart rate to an extent depending on dose, decreased diastolic blood pressure, end systolic diameter, and end systolic wall stress, and enhanced fractional shortening and cardiac output. Heart rate corrected pre-ejection period was shortened and left ventricular ejection time was prolonged, whereas electromechanical systole remained virtually unchanged. Autonomic blockade eliminated dihydralazine's effect on heart rate and cardiac output; blood pressure and systolic wall stress fell appreciably, whereas dihydralazine-induced changes in the systolic time intervals were virtually unaffected. Thus the present study indicates that regardless of the autonomic reflexes heart rate corrected pre-ejection period and left ventricular ejection time, but not electromechanical systole, are highly dependent on afterload, and this effect should be considered when systolic time intervals are evaluated.

Autonomic Nerve Block↗
PubMed2000

Modified heart-lung preparation for the evaluation of systolic and diastolic coronary flow in rats.

A modified heart-lung preparation of the rat, which permits measuring systolic and diastolic coronary flow separately and enables coronary compliance to be evaluated, is described. The systemic circulation was substituted by a shunt circuit, and the elastic properties of the arterial tree were mimicked by a rubber balloon. Systolic and diastolic coronary flow was evaluated from the pulmonary and aortic flow signal. Integrated phasic pulmonary flow represented right ventricular stroke volume. Integrated phasic systolic aortic flow represented left ventricular stroke volume minus that volume flowing into the coronary arteries during systole, because the aortic flow probe had to be inserted distal to the origin of the coronary vessels. Because right and left ventricular stroke volume was identical under steady-state conditions, the difference between systolic pulmonary and systolic aortic flow resulted in systolic coronary flow. Diastolic coronary flow was measured by means of the retrograde flow through the aortic flow probe. Coronary compliance was calculated according to Frank's windkessel model from coronary resistance and from central diastolic aortic pressure, which decayed exponentially after switching out the rubber balloon and the shunt circuit. It could be shown that the proportion of systolic to diastolic coronary flow depends on coronary compliance.

Animals↗
PubMed1999

Nonischemic end-systolic performance. Effect of alterations in regional and global left ventricular contractility.

Nonischemic end-systolic performance decreases during ischemia. These changes in performance are likely to be dependent on the size and site of the ischemic zone, as well as the prevailing loading conditions. This study was designed to examine the effect of regional and generalized changes in inotropy on nonischemic end-systolic performance, independent of the ischemic zone size. Twenty dogs were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure-thickness relationship data were obained during vena-caval balloon inflation. Measurements were obtained before and 90 s after left circumflex (LC) artery occlusion. Then, simultaneous with the occlusion of the LC artery, isoproterenol (0.04 microg/ml) was infused into the left anterior descending artery. After recovery, the same protocol was repeated before and after propranolol (0.5 mg/kg). In a separate set of animals, the same measurements were made following 2.5 and 5 microg/kg/min dobutamine. The effect of ischemia on the nonischemic end-systolic pressure-thickness relationship was expressed as the extent to which the relationship is shifted to the left. Infusion of intracoronary isoproterenol into the perfusion bed of the nonischemic zone produced a significant increase in the slope of the end-systolic pressure-thickness relationship. During ischemia, however, the extent of leftward shift of this relationship was less than that following beta-blockade. Intravenous dobutamine resulted in a dose-dependent increase in the slope of the nonischemic end-systolic pressure thickness relationship, but the extent of leftward displacement of the relationship in response to regional ischemia was less than that following the control occlusion. The nonischemic segment is coupled with the nonfunctioning ischemic zone in such a way that it is required of the nonischemic segment to operate at decreased end-systolic thickness for any end-systolic pressure, the extent of which is to be determined, in part, by the size of the ischemic zone and the contractile state of the nonischemic myocardium. The lower the contractile state prior to coronary occlusion the greater extent of leftward shift of the pressure-thickness relationship.

Animals↗
PubMed1982

Quantitative analysis of segmental wall motion throughout systole and diastole in the normal human left ventricle.

We traced left ventricular contours, frame-by-frame throughout systole and diastole, of normal sinus beats from 30 degrees right anterior oblique ventriculograms from 32 normal patients. We separated both systole and diastole into 19 equal time intervals each and calculated regional lengths (R), normalized by both end-diastole length and relative time interval (T) in systole and diastole and diastole, for the middle inferior wall, distal inferior wall, apex, distal anterior wall, middle anterior wall, and proximal anterior wall. We also computed the relative velocities of R, delta R/ delta T, over each quarter of systole and diastole. Comparing systole with diastole, we found significant differences between paired values of R at all regions except the distal inferior wall, but these differences were not the same between regions. Between regions, mean R and delta R/ delta T values were significantly different as early as the first quarter of systole. Within a region, there were significant differences between mean R and delta R/ delta T values over intervals as short as one-fourth of systole or diastole. Thus, there is no homogeneity between regions in normal wall motion in both systole and diastole. This normal lack of homogeneity has important clinical implications for identifying abnormal wall motion in individual patients from ventriculographic measurements, and for using the information present in the diastole portion of the ventriculogram to characterize normal segmental function.

Age Factors↗
PubMed1983

Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy.

Dynamic obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two-dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with two-dimensional echocardiography in views of the left ventricle obtained from the apex. At end-diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the "residual" distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy-myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet.

Adolescent↗
PubMed1985

Simultaneous assessment of left ventricular systolic and diastolic dysfunction during pacing-induced ischemia.

Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1986

Assessment of the end-systolic pressure-volume relationship in human beings with the use of a time-varying elastance model.

The analysis of left ventricular end-systolic pressure-volume relationships in human beings has been hindered by the lack of a practical method of serial volume assessment and by an imprecise definition of end-systole. Modifications of the end-systolic relationship that have been used to circumvent these problems have included the use of single-point end-systolic pressure-volume ratios, the use of peak systolic pressure/minimum ventricular volume points for end-systolic points, and the use of end-ejection as a marker for end-systole. To assess the correlation between the parameters generated by these modifications with the slope (Emax) and volume intercept (VO) of the end-systolic line as defined by Sagawa's model of time-varying elastance, simultaneous measurement of left ventricular pressure and gated radionuclide volume was made in 26 patients under various loading conditions and pressure-volume diagrams were constructed for each loading condition from 32 simultaneous pressure-volume coordinates. Two pressure-volume diagrams were recorded in 14 patients and three pressure-volume diagrams were recorded in 12 patients. Emax and VO were determined in all patients from the slope and volume intercept of the isochronic pressure-volume line with the maximum time-varying elastance as described by Sagawa's model and were designated true Emax and true VO, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1988

Effects of load alteration and coronary perfusion pressure on regional end-systolic relations.

Left ventricular end-systolic pressure-wall thickness and pressure-segment length relations have been used to assess regional myocardial contractility. The purpose of these studies was to determine whether the method of afterload alteration, coronary perfusion pressure, and the definition of end systole affected regional end-systolic relations. In paced open-chest pig hearts (n = 10), left ventricular pressure, wall thickness, and segment length were measured during vena caval occlusions. First, regional end-systolic relations were obtained before and after an increase in afterload with intravenous phenylephrine. This comparison was performed with the coronary circulation intact (closed loop) and with coronary perfusion pressure controlled extracorporeally (open loop). Second, with the open-loop preparation, the independent effect of a range of coronary perfusion pressures (45-155 mm Hg) on end-systolic relations was assessed. In both procedures, end systole was defined by the maximal isochronal slope, termed regional Emax, and by the maximal ratio of left ventricular pressure to regional dimension, termed Ees. In the first procedure, the slope and x-axis intercept of regional Emax were unchanged with phenylephrine. In contrast, the slope of Ees decreased with phenylephrine, consistent with a decrease in contractility. The extrapolated x-axis intercept of Ees shifted in a direction consistent with an increase in contractility. In the second procedure, increases in coronary perfusion pressure did not affect regional Emax but increased the slope of Ees. A decrease in the coronary perfusion pressure, particularly with ischemia, shifted the x-axis intercepts of both Emax and Ees in a direction consistent with a decrease in contractility. Thus, regional end-systolic relations in intact hearts are dependent on the method of afterload alteration and the coronary perfusion pressure. Furthermore, Emax differs from Ees, so the assessment of regional relations depends on how end systole is defined.

Animals↗
PubMed1991

Quantification of and correction for left ventricular systolic long-axis shortening by magnetic resonance tissue tagging and slice isolation.

BACKGROUND: Measurement of regional left ventricular (LV) function is predicted on the ability to compare equivalent LV segments at different time points during the cardiac cycle. Standard techniques of short-axis acquisition in two-dimensional echocardiography, cine computed tomography, and standard magnetic resonance imaging (MRI) acquire images from a fixed plane and fail to compensate for through-plane motion. The shortening of the left ventricle along its long axis during systole results in planar images of two different levels of the ventricle, leading to error in any derived functional measurements. LV systolic long-axis motion was measured in 19 normal volunteers using MRI. METHODS AND RESULTS: With a selective radio frequency (RF) tissue-tagging technique, three short-axis planes were labeled at end diastole and standard spin-echo images were acquired at end systole in the two- and four-chamber orientations. Persistence of the tags through systole allowed visualization of the intersecting short-axis tags in the long-axis images and allowed precise quantification of long-axis motion of the septum, lateral, anterior, and inferior walls at the base, mid, and apical LV levels. The total change in position along the long axis between end diastole and end systole was greatest at the base, which moved toward the apex 12.8 +/- 3.8 mm. The mid left ventricle moved 6.9 +/- 2.6 mm, and the apex was nearly stationary, moving only 1.6 +/- 2.2 mm (p less than 0.001). Having quantified the normal range of long-axis shortening, we developed a technique that isolates a slice of tissue between selective RF saturation planes at end diastole. Combining this with a wide end-systolic image slice, end-systolic images were acquired without contamination of signal from adjacent tissue moving into the imaging plane. This technique was validated in a moving phantom and in normal volunteers. CONCLUSIONS: Significant LV systolic long-axis shortening exists, and this effect is seen the most at the base and the least at the apex. At a given ventricular level, shortening varied significantly according to location. A method using selective saturation pulses and gated spin-echo MRI automatically corrects for this motion and thus eliminates misregistration artifact from regional function analysis.

Evaluation Studies as Topic↗
PubMed2004

Familial and genomic analyses of postural changes in systolic and diastolic blood pressure.

The physiological adaptation to the erect posture involves integrated neural and cardiovascular responses that might be determined by genetic factors. We examined the familial- and individual-specific components of variance for postural changes in systolic and diastolic blood pressure in 767 volunteer nuclear adult families from the Victorian Family Heart Study. In 274 adult sibling pairs, we made a genome-wide scan using 400 markers for quantitative trait loci linked with the postural changes in systolic and diastolic pressures. Overall, systolic pressure did not change on standing, but there was considerable variation in this phenotype (SD=8.1 mm Hg). Familial analyses revealed that 25% of the variance of change in systolic pressure was attributable to genetic factors. In contrast, diastolic pressure increased by 6.3 mm Hg (SD=7.0 mm Hg) on standing and there was no evidence of contributory genetic factors. Multipoint quantitative genome linkage mapping suggested evidence (Z=3.2) of linkage of the postural change in systolic pressure to chromosome 12 but found no genome-wide evidence of linkage for the change in diastolic pressure. These findings suggest that genetic factors determine whether systolic pressure decreases or increases when one stands, possibly as the result of unidentified alleles on chromosome 12. The genetics of postural changes in systolic blood pressure might reflect the general buffering function of the baroreflex; thereby, the predisposition to sudden decreases or increases in systolic pressure might cause postural hypotension or vessel wall disruption, respectively.

Adult↗