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PubMed1984

Vasodilator effect on right ventricular function in congestive heart failure and pulmonary hypertension: end-systolic pressure--volume relation.

The right ventricular (RV) end-systolic pressure-volume relation during vasodilator administration was studied in 10 patients with pulmonary arterial (PA) hypertension, most of whom had biventricular failure. RV end-systolic volumes were estimated from equilibrium radionuclide RV counts and forward cardiac output. Simultaneous radionuclide and hemodynamic values were measured at rest and during nitroglycerin and nitroprusside infusion. Vasodilator administration resulted in decreases in PA mean and systolic pressures in all 10 patients, with an average decrease in end-systolic pressure (p less than 0.001) from 48 +/- 11 to 38 +/- 9 and 35 +/- 10 mm Hg during nitroglycerin and nitroprusside administration, respectively. In each patient, a direct linear relation was observed between the vasodilator-induced decrease in PA end-systolic pressure and in RV end-systolic volume. Average RV end-systolic volume decreased (p less than 0.001), from 130 +/- 69 ml/m2 at baseline to 108 +/- 62 and 102 +/- 55 ml/m2 during nitroglycerin and nitroprusside infusion, respectively. The slope of the RV end-systolic pressure-volume relation was directly related to RV ejection fraction. Thus, the vasodilator-induced decrease in PA systolic pressure is accompanied by a linear decrease in RV end-systolic volume, with a slope which is dependent on RV systolic function. This linear relation is analogous to the left ventricular end-systolic pressure-volume relation.

Adult↗

PubMed2001

Similar effects of isolated systolic and combined hypertension on left ventricular geometry and function: the LIFE Study.

Echocardiograms of 143 patients with isolated systolic hypertension were compared to 808 patients with combined (systolic and diastolic) hypertension. All patients met electrocardiographic criteria for left ventricular hypertrophy and were evaluated off medication. Patients with isolated systolic hypertension were older, shorter, weighed less, and were mostly women, but body mass index (BMI) was similar in both groups. Systolic blood pressure (SBP) was 172 mm Hg in isolated systolic hypertension, 174 mm Hg in combined (P = not significant). Diastolic blood pressure was 83 and 101 mm Hg, respectively (P < .001). Despite having mean arterial pressure 12 mm Hg lower than patients with combined hypertension, the group with isolated systolic hypertension had equally severe abnormalities of left ventricular mass, left ventricular geometric patterns, and measures of systolic and diastolic function. Peripheral resistance was lower and pulse pressure/stroke volume ratio (arterial stiffness index) was higher and the isovolumic relaxation time shorter in isolated systolic hypertension. Multiple regression analyses identified age, height, BMI, stress-corrected mid wall shortening, stroke volume, male gender, and systolic or mean blood pressure (but not isolated systolic hypertension) as independent correlates of left ventricular mass. Relative wall thickness was independently associated with isolated systolic hypertension (P = .001) in addition to mean pressure and other covariates. The present results add support to the concept that systolic blood pressure (SBP) is a stronger determinant than diastolic pressure of cardiac target organ damage in hypertension.

Aged↗

PubMed1987

Post-systolic shortening: a marker of potential for early recovery of acutely ischaemic myocardium in the dog.

Regional diastolic wall motion was studied with sonomicrometry in 30 open chest anaesthetised dogs after left anterior descending stenosis or occlusion. Post-systolic shortening and thickening, defined as the magnitude of segment shortening or wall thickening that occurred after end systole, was measured in peripheral and central ischaemic segments. These post-systolic events developed concurrently with impaired systolic shortening or thickening, either immediately after acute coronary occlusion or during progressive stenosis, and persisted with the development of dyskinesis and during reperfusion. The magnitude of these events in dyskinetic segments of 24 dogs was considerable, reaching 50(2)% (mean(SEM)) and 33(3)% of shortening or thickening that was present before coronary occlusion. Post-systolic shortening and thickening were maximum at 100(2) ms after peak negative dP/dt. Significant correlations were found between systolic shortening or thickening before coronary occlusion and post-systolic shortening (r = 0.74, 56 segments) or thickening (r = 0.84, 19 segments) after occlusion, but there was no correlation between post-systolic shortening or thickening and dyskinetic lengthening or thinning. In seven dogs followed for 4 h after coronary occlusion post-systolic shortening fell by 15% in peripheral segments and by 70% in central segments (p less than 0.002). In 17 dogs reperfused after 60 (n = 9) or 90 (n = 8) min of coronary occlusion the maximal recovery of systolic shortening early after reperfusion was significantly related to the magnitude of post-systolic shortening immediately before reperfusion (60 min occlusion r = 0.84, 90 min occlusion r = 0.88). These data show that post-systolic shortening is a marker of potential for early recovery of function of acutely ischaemic myocardium and suggest that it is due, at least in part, to an active process.

Acute Disease↗

PubMed1995

Effects of systolic anterior motion of the mitral valve on haemodynamics. Evaluation by a direct method.

We evaluated the effects of systolic anterior motion systolic anterior motion of the mitral valve on cardiac haemodynamics. Seven adult mongrel dogs in which systolic anterior motion-septal contact was observed after dobutamine administration were used. To exclude the effects of left ventricular function and morphology, a stone removal basket catheter was placed in the left ventricular outflow tract, and haemodynamics were compared with the basket closed and opened. The basket was opened five times in three dogs not showing systolic anterior motion-septal contact, but the basket itself did not effect the haemodynamics. In the seven dogs that showed systolic anterior motion-septal contact without left ventricular hypertrophy, the basket was opened a total of 33 times in the presence of various degrees of systolic anterior motion-septal contact. After opening the basket, systolic anterior motion was reduced echocardiographically, and significant (P<0.01) changes were observed in the left ventricle-aorta pressure gradient (from 68 +/- 22 to 25 +/- 15 mm Hg), the systolic ejection period (from 146 +/- 19 to 135 +/- 16 ms), and the stroke volume (SV; from 9.4 +/- 2.9 to 10.1 +/- 3.3 ml). After basket inflation, aortic pressure and aortic flow waveforms changed but the peak pressure and flow velocity did not. The temporal distribution of left ventricular ejection also definitely changed after the basket was opened. No changes were observed in the peak dp/dt, peak negative dp/dt, time constant, left ventricular end-diastolic pressure, or left atrial pressure. These observations in this animal model of systolic anterior motion without left ventricular hypertrophy suggest that: (1) there is no potential for generation of an intra-cavity gradient in the absence of systolic anterior motion of the mitral valve, so that (2) systolic anterior motion narrowed the left ventricular outflow tract and, consequently, produced the systolic ejection period, and affected the left ventricular ejection dynamics, and that (3) the basket catheter is useful because it allows these assessments in the same heart with a nearly fixed left ventricular contractility, at least in our animal model.

Animals↗

PubMed1995

Haemodynamic basis for the development of left ventricular failure in systolic hypertension and for its logical therapy.

In youth, properties of the human arterial system are such that pulse pressure generated by ventricular ejection is low, and the major component of wave reflection returns to the heart after the aortic valve has shut, so making no contribution to ventricular load, but boosting pressure throughout diastole and so aiding coronary perfusion. That constitutes optimal arterial function and optimal vascular/ventricular interaction. With ageing, the aorta and elastic arteries stiffen, so that aortic pulse pressure is markedly increased. This is a consequence of a direct stiffening effect on the aorta itself, and of an indirect effect caused by early return of wave reflection consequent upon stiffening of the whole arterial system with an increase in its pulse wave velocity. There is a change in contour of the aorta pressure wave with wave generation of a late systolic peak and disappearance of the diastolic wave; the reflected wave moves from diastole and systole. Because the lowest diastolic pressure remains relatively constant [1,10], increased pulse pressure causes a substantial increase in aortic systolic pressure. Increased aortic systolic pressure is associated with increased left ventricular pressure and leads to left ventricular hypertrophy. Sustained elevation in systolic pressure and persistent left ventricular hypertrophy are associated with progressive degenerative changes in the hypertrophied myocytes such that these weaken, developing less force with each contraction. The weakened, hypertrophied fibres lengthen and the ventricle dilates, with force and cardiac output initally being maintained at greater muscle length and ventricular volume through the Frank-Starling mechanism. Ultimately compensation is lost. The hypertrophied ventricle normally functions as a flow source, which is capable of generating flow even against very high pressure. With the development of cardiac failure through muscle weakening, the ventricle comes to act as a pressure source, with ventricular output very sensitive to pressure and to changes in pressure. The normal ventricle functions in an intermediate position, even though it is closer in behaviour to a flow than to a pressure source. Wave reflection adds to pressure but subtracts from flow. In youth, wave reflection returns to the heart during diastole when the aortic valve is shut. Negative flow is not possible, so wave reflection is apparent only as a secondary pressure wave in the ascending aorta. In older subjects, when the left ventricle is beating powerfully, return of wave reflection during systole has less obvious an effect on the ascending aortic flow wave, but causes an obvious secondary boost to pressure in the ascending aorta and left ventricle. Hence, under normal circumstances, wave reflection at the heart is apparent as a positive secondary pressure wave, either because the aortic valve is shut when this wave returns, or because the ventricle possesses enough power that it virtually overcomes any negative influence on flow when reflection returns during systole. When the myocardium weakens and the heart fails, the heart starts to behave like a pressure source, and wave reflection starts to have a far greater effect on flow; wave reflection is manifested more as a negative influence on flow than as a positive influence on pressure. As heart failure develops, there is a progressive change in flow wave contour, with early deceleration of aortic flow and ultimately, abbreviation of systolic ejection duration with fall in stroke volume. Early wave reflection is the major factor in the genesis of systolic hypertension. Early wave reflection remains a major factor when heart failure develops, although its effect is apparent in reduction of late systolic flow rather than as a boost to late systolic pressure. Reduction in wave reflection through use of vasodilatory agents is a logical strategy in treatment of systolic hypertension. That type of therapy is equally logical in treatment

Animals↗

PubMed1999

Systolic blood pressure within an intermediate range may reduce memory loss in an elderly hypertensive cohort.

The objective of this study was to determine if maintenance of systolic blood pressure (BP) within a high range or low range among treated hypertensive patients increases the risk of memory decline. Biennial neuropsychological evaluations were performed on 158 hypertensive subjects. Decline/year was measured on the Cued Selective Reminding test (total free recall and delayed recall) in three systolic BP groups (low-i.e., mean systolic BP during the follow-up period < 135 mm Hg; intermediate-i.e., 135 mm Hg < or = mean systolic BP < or = 150 mm Hg; high-i.e., mean systolic BP > 150 mm Hg). In total free recall, the three systolic BP groups had significantly different declines per year (P = .02), with patients in the high subgroup showing the greatest decline. In delayed recall, the three systolic BP groups also showed significantly different declines per year (P = .04), with patients in the low subgroup having the greatest decline. Chronically elevated systolic BP > 150 mm Hg is associated with accelerated memory decline compared to older treated hypertensive patients with systolic BP in an intermediate range. Chronically maintained systolic BP within a low normal range < 135 mm Hg in older treated hypertensive subjects may be associated with accelerated memory decline, specifically in a test of delayed memory recall, compared to patients with systolic BP in an intermediate range. Optimal regulation of systolic BP may be a potential modifiable risk factor to prevent or minimize memory loss in older hypertensive patients.

Aged↗

PubMed2003

Left ventricular systolic performance during prolonged strenuous exercise in female triathletes.

BACKGROUND: The effect of prolonged strenuous exercise (PSE) on left ventricular (LV) systolic function has not been well studied in younger female triathletes. This study examined LV systolic function prior to, during and immediately following PSE (i.e., 40 km bicycle time trial followed by a 10 km run) in 13 younger (29 PlusMinus; 6 years) female triathletes. METHODS: Two-dimensional echocardiographic images were obtained prior to, at 30-minute intervals during and immediately following PSE. Heart rate, systolic blood pressure, end-diastolic and end-systolic cavity areas were measured at each time point. Echocardiographic and hemodynamic measures were also combined to obtain LV end-systolic wall stress and myocardial contractility (i.e., systolic blood pressure - end-systolic cavity area relation). RESULTS: Subjects exercised at an intensity equivalent to 90 PlusMinus; 3% of maximal heart rate. Heart rate, systolic blood pressure, systolic blood pressure - end-systolic cavity area relation and fractional area change increased while end-diastolic and end-systolic cavity areas decreased during exertion. CONCLUSIONS: PSE is associated with enhanced LV systolic function secondary to an increase in myocardial contractility in younger female triathletes.

Journal Article↗

PubMed2001

The benefit of treating isolated systolic hypertension.

Isolated systolic hypertension affects over 15% of all people older than 60 years of age. In the elderly, systolic hypertension is a major modifiable cardiovascular risk factor. Systolic blood pressure is associated with higher risk of an adverse outcome. Diastolic blood pressure is inversely correlated with total mortality, independent of systolic blood pressure, highlighting the role of pulse pressure as risk factor. Three placebo-controlled outcome trials on antihypertensive drug treatment in older patients with isolated systolic hypertension have been published: the Systolic Hypertension in the Elderly Program (SHEP), the Systolic Hypertension in Europe (Syst-Eur) Trial, and the Systolic Hypertension in China (Syst-China) Trial. These three trials showed the benefit of antihypertensive drug treatment. A meta-analysis was done by pooling the patients from these three trials with a subset of patients with isolated systolic hypertension from five other trials in the elderly. The pooled results of 15,693 older patients with isolated systolic hypertension prove that antihypertensive drug treatment is justified if systolic blood pressure on repeated clinic measurements is 160 mm Hg or higher.

Aged↗

PubMed2006

Right ventricular systolic function is not the sole determinant of tricuspid annular motion.

Maximal tricuspid annular plane systolic excursion (TAPSE) correlates well with right ventricular (RV) function; however, little is known regarding the impact of left ventricular (LV) systolic function on TAPSE. Consequently, TAPSE was examined in 206 patients (105 men; mean age 56 +/- 17 years), and the data were analyzed with respect to RV (RV fractional area change 45 +/- 19%) and LV (56 +/- 17%) systolic function. The mean TAPSE for the population studied was 1.97 +/- 0.72 cm. Although a strong linear correlation was noted between RV fractional area change and TAPSE (r = 0.73, p <0.0001), relative differences with regard to TAPSE were also found. First, the greatest TAPSE was noted only when RV and LV systolic function were normal (2.46 +/- 0.50 cm). Second, patients with reduced RV systolic function had the smallest TAPSE (1.28 +/- 0.48 cm, p <0.0001). Third, patients with normal RV function but reduced LV systolic function had TAPSE (1.91 +/- 0.54 cm, p <0.0001) that was intermediate between that of patients with normal RV and LV systolic function and those with abnormal RV systolic function. Fourth, patients with reduced biventricular function had the smallest TAPSE (1.16 +/- 0.41 cm, p <0.0001). In conclusion, TAPSE is not only determined by RV systolic function but also appears to depend on LV systolic function. TAPSE <2.0 cm is associated with some degree of either RV or LV dysfunction, whereas a value >2.0 cm suggests normal biventricular systolic function.

Adult↗

PubMed2006

Systolic anterior motion after mitral valve repair: is surgical intervention necessary?

OBJECTIVE: The natural history and management of patients with systolic anterior motion after mitral valve repair are uncertain. METHODS: We performed a retrospective chart review and survey follow-up of all patients in whom systolic anterior motion developed intraoperatively after mitral valve repair. RESULTS: From January 1993 to December 2002, mitral valve repair was performed in 2076 patients, and in 174 cases (8.4%) systolic anterior motion was identified on intraoperative echocardiography. These patients form the study group. Initially, patients were managed with a combination of beta-blockade, vasoconstriction with phenylephrine, and/or intravascular volume expansion. Four patients had revision of repair because of persistent systolic anterior motion, and 3 additional patients had revision of repair because of mitral regurgitation from other causes. The median follow-up of the remaining 167 patients was 5.4 years (range 0-13.2 years). There were 2 late reoperations, but none were caused by systolic anterior motion or left ventricular outflow tract obstruction. Ninety percent of patients were in New York Heart Association class I, 7% were in class II, and 3% were in class III or IV. Echocardiograms were available for review in 93 patients at a median interval of 5.4 years (range 0.2-12.2 years); 13 patients had systolic anterior motion, and 4 patients had systolic anterior motion with left ventricular outflow tract obstruction. CONCLUSIONS: In this experience, most cases of systolic anterior motion resolved with conservative measures including beta-blockade, vasoconstriction, and fluid administration. Persistent systolic anterior motion with left ventricular outflow tract obstruction was documented in 2.3% of patients who had early systolic anterior motion, but late reoperation was not required. Furthermore, the clinical outcomes of patients with systolic anterior motion are comparable to the current norms for mitral valve repair. Ninety percent of patients were in New York Heart Association class I, 7% were in class II, and 3% were in class III or IV.

Adult↗

PubMed2001

Benefits of antihypertensive drug treatment in elderly patients with isolated systolic hypertension.

Isolated systolic hypertension affects over 15% of all people older than 60 years. In the elderly, systolic hypertension is a major modifiable cardiovascular risk factor. Systolic blood pressure is associated with higher risk of an adverse outcome, whereas diastolic blood pressure is inversely correlated with total mortality, independent of systolic blood pressure, highlighting the role of pulse pressure as risk factor. Three placebo-controlled outcome trials on antihypertensive drug treatment in older patients with isolated systolic hypertension have been published: the Systolic Hypertension in the Elderly Program (SHEP), the Systolic Hypertension in Europe (Syst-Eur) Trial and the Systolic Hypertension in China (Syst-China) Trial. These three trials demonstrated the benefit of antihypertensive drug treatment. A meta-analysis was performed by pooling the patients from these three trials with a subset of patients with isolated systolic hypertension from five other trials in the elderly. Antihypertensive treatment based on a calcium-channel blocker may provide additional benefits in diabetic patients and in the prevention of dementia and renal dysfunction. The pooled results of 15693 older patients with isolated systolic hypertension prove that antihypertensive drug treatment is justified if on repeated clinic measurements systolic blood pressure is 160 mmHg or higher.

Aged↗

PubMed2000

Effects of first myocardial infarction on left ventricular systolic and diastolic function with the use of mitral annular velocity determined by pulsed wave doppler tissue imaging.

This study was undertaken to assess the effect of a first myocardial infarction (MI) on the systolic and diastolic velocity profiles of the mitral annulus determined by pulsed wave Doppler tissue imaging and thereby evaluate left ventricular (LV) function after MI. Seventy-eight patients with a first MI were examined before discharge. Peak systolic, peak early diastolic, and peak late diastolic velocities were recorded at 4 different sites on the mitral annulus corresponding to the septum, anterior, lateral, and inferior sites of the left ventricle. In addition, the amplitude of mitral annular motion at the 4 above LV sites, the ejection fraction, and conventional Doppler diastolic parameters were recorded. Nineteen age-matched healthy subjects served as controls. Compared with healthy subjects, the MI patients had a significantly reduced peak systolic velocity at the mitral annulus, especially at the infarction sites. A relatively good linear correlation was found between the ejection fraction and the mean systolic velocity from the 4 LV sites (r = 0.74, P <.001). The correlation was also good when the mean peak systolic mitral annular velocity was tested against the magnitude of the mean mitral annular motion (r = 0.77, P <.001). When the patients were divided into 2 different groups with respect to an ejection fraction > or =0.50 or <0.50, a cutoff point of mean systolic mitral annular velocity of > or =7.5 cm/s had a sensitivity of 79% and a specificity of 88% in predicting a preserved global LV systolic function. Similar to systolic velocities, the early diastolic velocity was also reduced, especially at the infarction sites. The peak mitral annular early diastolic velocity correlated well with both LV ejection fraction (r =.66, P <.001) and mean systolic mitral annular motion (r = 0.68, P <.001). However, no correlation existed between the early diastolic velocity and conventional diastolic Doppler parameters. The reduced peak systolic mitral annular velocity seems to be an expression of regionally reduced systolic function. The peak early diastolic velocity is also reduced, especially at the infarction sites, and reflects regional diastolic dysfunction. Thus, quantification of myocardial velocity by Doppler tissue imaging opens up a new possibility of assessing LV function along its long axis.

Blood Flow Velocity↗

PubMed2006

Is post-systolic shortening a reliable indicator of myocardial viability? An MR tagging and late-enhancement study.

PURPOSE: In ischemic myocardium systolic strain is reduced and followed by a deformation after systole, the so-called post-systolic shortening. The presence of post systolic shortening is therefore considered a marker of viability even though its mechanism remains unclear. The hypothesis was tested whether post-systolic shortening might be a passive recoil phenomenon and therefore not uniquely associated with viability. METHODS: Five patients with a history of myocardial infarctions and fully transmural scars in late enhancement imaging and five age-matched healthy volunteers underwent a tagging study to analyze systolic and post-systolic deformation in transmurally infarcted and contra-lateral non-infarcted myocardium. From CSPAMM myocardial tagging data, mid-wall circumferential fiber shortening, radial displacement, and rotation parameters were semi-automatically extracted by harmonic phase (HARP). RESULTS: In transmurally infarcted myocardium, a post systolic shortening of 6.2 +/- 1.8% was present occurring in early diastole (time to maximum circumferential fiber shortening increased versus both, contralateral myocardium and corresponding sectors in healthy volunteers, p < 0.01). Maximum radial displacement was decreased in scar tissue (p < 0.001 versus contra-lateral), but time to maximum radial displacement did not differ. Rotation did not discriminate between infarcted and non-infarcted myocardium. CONCLUSIONS: The pure finding of post-systolic shortening is not sufficient for the diagnosis of residual myocardial viability. Post-systolic shortening may be explained in part by passive recoil, which releases energy stored in the scar tissue during systolic intra-ventricular unloading. Circumferential fiber shortening appears best suited for characterization of regional deformation, whereas radial displacement and rotation are more dependent on tethering effects, and thus, are more likely to reflect global chamber mechanics.

Analysis of Variance↗

PubMed2004

A novel method to assess systolic ventricular function using atrioventricular plane displacement--a study in young healthy males and patients with heart disease.

Analysis of atrioventricular plane displacement (AVPD) is a well established method for assessment of both systolic and diastolic ventricular function. For several years, AVPD has been a clinical tool and there are many current, as well as potential, areas of application. However, clinical work has shown that the traditional method for evaluation of systolic ventricular function, called total AVPD, does not temporally reflect true systole. Systolic AVPD is a new approach for measuring AVPD to assess ventricular systolic function. We wished to apply this new model in healthy subjects and in patients with different common heart diseases. Twenty-eight young healthy males and 30 patients (aortic stenosis, left sided regurgitant lesions, postmyocardial infarction) were enrolled. AVPD was obtained at the four standard sites by M-mode. Total AVPD was measured in the conventional way and systolic AVPD by identifying true systole, by means of mitral- and aortic valve closure respectively. Ventricular volumes were calculated according to biplane Simpson's rule. The systolic AVPD measurements were significantly lower than the total measurements, at both atrioventricular planes in all groups (P<0.001). This discrepancy was greater at the mitral than at the tricuspid annulus in the patients 24.2% vs. 15.5% (P<0.001), but did not differ in the healthy subjects. At the mitral annulus, this discrepancy also seemed to be more pronounced in the patients than in the healthy subjects 24.2% vs. 10.7%. When assessing ventricular systolic function by AVPD, the conventional method overestimates the amplitude in relation to true systolic function in both patients with heart disease and in young healthy males. Thus, there are uncertainties regarding earlier estimations of AVPD in terms of expression of systolic function and regarding previously presented reference values. We recommend the proposed methodology.

Adult↗

PubMed1998

Systolic coronary flow impediment in the dog: role of ventricular pressure and contractility.

The present study was planned to investigate the effect of left ventricular pressure and inotropic state on coronary arterial inflow in systole in the anaesthetized dog. A wide range of left ventricular systolic pressures, including the physiological range, were studied. Experiments were done under conditions of maximal vasodilatation and low perfusion pressure in order to avoid vascular autoregulative interference and to keep the microvascular pressure within the normal range. In five anaesthetized dogs, perfused with extracorporeal circulation system, ventricular volume was changed from 20 to 50 ml in steps of 10 ml by filling an intraventricular latex balloon, and the related changes in left ventricular pressure and coronary flow were measured. The volume was then extended to 70 ml to obtain an overstretch which induced a transient decrease in cardiac contractility. During the period of low cardiac contractility the volume was brought back to 20 ml in steps of 10 ml. Systolic ventricular pressure changed with volume but was lower during the period of low contractility. For systolic pressures below 100 mmHg there was no significant relationship between pressure and coronary systolic flow, but the relationship shifted to higher flows during low contractility. For systolic pressures above 100 mmHg systolic coronary flow decreased significantly when systolic pressure increased. In this case the slopes of the relationships were not significantly different before and after the reduction in contractility. These findings suggest that for systolic pressures less than 100 mmHg (i.e. below the physiological range) the shielding effect of the contracting ventricle prevents the ventricular pressure from being transmitted in the myocardial wall. When systolic pressure exceeds 100 mmHg the shielding effect is overcome and the amplitude of the systolic flow reduction varies with ventricular pressure.

Acid-Base Equilibrium↗

PubMed2002

"Diastolic heart failure" or heart failure caused by subtle left ventricular systolic dysfunction?

OBJECTIVES: To determine whether patients with suspected heart failure but preserved systolic function, as determined by conventional echocardiographic measures (often said to have "diastolic heart failure), might have subtle left ventricular systolic dysfunction detectable by a new measure of left ventricular systolic function-left ventricular systolic atrioventricular plane displacement. DESIGN: Observational study. SETTING: Direct access echocardiography. PATIENTS: 147 patients with suspected heart failure referred by general practitioners. MEASUREMENTS: Echocardiographic assessment of conventional measures of left ventricular systolic function (fractional shortening, ejection fraction (by Simpson's biplane method) and "eyeball" assessment) and measurement of left ventricular systolic atrioventricular plane displacement. RESULTS: Between 21% and 33% of patients with "normal" left ventricular systolic function by conventional methods were found to have abnormal left ventricular systolic atrioventricular plane displacement. CONCLUSIONS: Approximately one quarter of patients with suspected heart failure but preserved systolic function by conventional methods have abnormal atrioventricular plane displacement. These patients with suspected heart failure but preserved systolic function by conventional echocardiographic measures may have heart failure caused by subtle systolic dysfunction rather than isolated "diastolic heart failure".

Aged↗

PubMed2002

Left ventricular long axis function in diastolic heart failure is reduced in both diastole and systole: time for a redefinition?

OBJECTIVE: To test the hypothesis that, when measured in the long axis, left ventricular systolic function is abnormal in patients with diastolic heart failure. DESIGN: A case-control study. SETTING: University teaching hospital (tertiary referral centre). PATIENTS: 68 patients with heart failure, 29 with a left ventricular ejection fraction (LVEF) of > 0.45 and diastolic dysfunction (diastolic heart failure), 39 with an LVEF of </= 0.45 (systolic heart failure), and 105 normal subjects, including 33 age matched controls. METHODS: LVEF was measured by cross sectional Simpson's method, and mitral annular amplitudes and velocities by M mode and tissue Doppler echocardiography, respectively, along with mitral Doppler inflow velocities. Results were compared between the three groups. MAIN OUTCOME MEASURES: Peak systolic mitral annular velocity and amplitude between the different groups. RESULTS: The mitral annular peak mean velocity and amplitude in systole were lower in the patients with diastolic heart failure (mean (SEM), 4.8 (0.2) cm/s) than in the age matched normal controls (6.1 (0.14) cm/s), but higher than those with systolic heart failure (2.8 (0.13) cm/s) (all p < 0.001). Similar changes were seen the mitral annular amplitude during systole. Peak early diastolic velocity and amplitude were also significantly reduced in the group with diastolic heart failure. Left ventricular hypertrophy was evident in over 95% patients in both diastolic and systolic heart failure groups, with a comparable left ventricular mass index. CONCLUSIONS: In patients with diastolic heart failure and evidence of left ventricular hypertrophy, there is systolic left ventricular impairment as measured by myocardial Doppler imaging of the longitudinal axis. Thus subtle abnormalities of systolic function are present in patients with heart failure and a normal left ventricular ejection fraction, and there appears to be a continuum of systolic function between those with truly normal, mildly impaired (labelled diastolic heart failure), and obviously abnormal left ventricular systolic function. Isolated diastolic dysfunction is uncommon.

Adult↗

PubMed1990

Dissociation of end systole from end ejection in patients with long-term mitral regurgitation.

To determine whether left ventricular (LV) end systole and end ejection uncouple in patients with long-term mitral regurgitation, 59 patients (22 control patients with atypical chest pain, 21 patients with aortic regurgitation, and 16 patients with mitral regurgitation) were studied with micromanometer LV catheters and radionuclide angiograms. End systole was defined as the time of occurrence (Tmax) of the maximum time-varying elastance (Emax), and end ejection was defined as the time of occurrence of minimum ventricular volume (minV) and zero systolic flow as approximated by the aortic dicrotic notch (Aodi). The temporal relation between end systole and end ejection in the control patients was Tmax (331 +/- 42 [SD] msec), minV (336 +/- 36 msec), and then, zero systolic flow (355 +/- 23 msec). This temporal relation was maintained in the patients with aortic regurgitation. In contrast, in the patients with mitral regurgitation, the temporal relation was Tmax (266 +/- 49 msec), zero systolic flow (310 +/- 37 msec, p less than 0.01 vs. Tmax), and then, minV (355 +/- 37 msec, p less than 0.001 vs. Tmax and p less than 0.01 vs. Aodi). Additionally, the average Tmax occurred earlier in the patients with mitral regurgitation than in the control patients and patients with aortic regurgitation (p less than 0.01, for both), whereas the average time to minimum ventricular volume was similar in all three patient groups. Moreover, the average time to zero systolic flow also occurred earlier in the patients with mitral regurgitation than in the control patients (p less than 0.01) and patients with aortic regurgitation (p less than 0.05). Because of the dissociation of end systole from minimum ventricular volume in the patients with mitral regurgitation, the end-ejection pressure-volume relations calculated at minimum ventricular volume did not correlate (r = -0.09), whereas those calculated at zero systolic flow did correlate (r = 0.88) with the Emax slope values. We conclude that end ejection, defined as minimum ventricular volume, dissociates from end systole in patients with mitral regurgitation because of the shortened time to LV end systole in association with preservation of the time to LV end ejection due to the low impedance to ejection presented by the left atrium. Therefore, pressure-volume relations calculated at minimum ventricular volume might not be useful for assessing LV chamber performance in some patients with mitral regurgitation.

Chronic Disease↗