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PubMed2005

Deceleration time of systolic pulmonary venous flow: a new clinical marker of left atrial pressure and compliance.

The curvilinearity of the atrial pressure-volume curve implies that atrial compliance decreases progressively with increasing left atrial (LA) pressure (LAP). We predicted that reduced LA compliance leads to more rapid deceleration of systolic pulmonary venous (PV) flow. With this rationale, we investigated whether the deceleration time (t dec) of PV systolic flow velocity reflects mean LAP. In eight patients during coronary surgery, before extracorporeal circulation, PV flow by ultrasonic transit time and invasive LAP were recorded during stepwise volume loading. The t dec was calculated using two methods: by drawing a tangent through peak deceleration and by drawing a line from peak systolic flow through the nadir between the systolic and early diastolic flow waves. LA compliance was calculated as the systolic PV flow integral divided by LAP increment. Volume loading increased mean LAP from 11 +/- 3 to 20 +/- 5 mmHg (P < 0.001) (n = 40), reduced LA compliance from 1.16 +/- 0.42 to 0.72 +/- 0.40 ml/mmHg (P < 0.004) (n = 40), and reduced t dec from 320 +/- 50 to 170 +/- 40 ms (P < 0.0005) (n = 40). Mean LAP correlated well with t dec (r = 0.84, P < 0.0005) (n = 40) and LA compliance (r = 0.79, P < 0.0005) (n = 40). Elevated LAP caused a decrease in LA compliance and therefore more rapid deceleration of systolic PV flow. The t dec has potential to become a semiquantitative marker of LAP and an index of LA passive elastic properties.

Atrial Function, Left↗
PubMed2001

Prognostic implications of left ventricular diastolic dysfunction with preserved systolic function following acute myocardial infarction.

The contribution of diastolic dysfunction in patients with preserved left ventricular (LV) systolic function to impaired functional status and cardiac mortality in myocardial infarction (MI) is unknown. In the present study, assessment of LV diastolic function was performed by Doppler analysis of the mitral and pulmonary venous flow, and the propagation velocity of early mitral flow by color M-mode Doppler echocardiography in 183 consecutive patients at day 5-7 following their first acute MI. Patients were classified into four groups: group A: preserved LV systolic and diastolic function (n = 73); group B: LV systolic dysfunction with preserved diastolic function (n = 10); group C: LV diastolic dysfunction with preserved systolic function (n = 60); group D: combined LV systolic and diastolic dysfunction (n = 40). The cardiac mortality rate at 1 year was significantly higher in groups C (13%) and D (38%) compared to A (2%) (p < 0.01). Multivariate regression analysis identified LV diastolic dysfunction (p = 0.001), Killip class >or=II (p = 0.006), and age (0.008) as predictors of cardiac death or readmission due to heart failure. The presence of LV diastolic dysfunction with preserved systolic dysfunction is associated with increased morbidity and mortality following acute MI.

Aged↗
PubMed1987

Disparity between ejection and end-systolic indexes of left ventricular contractility in mitral regurgitation.

To examine left ventricular function in mitral regurgitation (MR), we compared the ejection phase indexes of left ventricular contractility with maximal systolic elastance (Emax) in an experimental preparation of MR. In eight anesthetized open-chest dogs, pressure-volume loops were derived during afterload manipulation with methoxamine and nitroprusside from simultaneous left ventricular pressure and dimensional (sonomicrometry techniques) data before and after creation of MR. From these data maximal systolic elastance (Emax), the end-systolic pressure-volume relationship (ESPVR), and the end-systolic stress-volume relationship (ESSVR) were determined by linear regression analysis. After creation of MR, end-diastolic volume increased significantly (40 +/- 13 to 53 +/- 18 ml, p less than .001); likewise end-systolic volume increased (28 +/- 11 to 33 +/- 15 ml, p less than .05). Ejection fraction increased after MR (35 +/- 6% to 44 +/- 8%, p less than .005), as did the mean velocity of fiber shortening (0.62 +/- 0.20 to 1.02 +/- 0.39 sec-1, p less than .02). In contrast, Emax declined significantly (4.63 +/- 2.5 to 3.54 +/- 1.94 mm Hg/ml, p less than .05); ESPVR and ESSVR showed similar directional changes. An inverse relationship was found between systolic elastance and end-diastolic volume in both control and MR states. When Emax, ESPVR, and ESSVR were normalized to end-diastolic volume, they were unchanged after MR. These results suggest that either there was a decline in left ventricular contractile state after MR, or that contractility was unchanged (if elastance is normalized for increased contractility, but occurred as a consequence of increased preload with no significant change in afterload.

Animals↗
PubMed1987

Hierarchy of levels of ischemia-induced impairment in regional left ventricular systolic function in man.

We tested the hypothesis that different subsets of ischemia-induced wall motion disorders are characterized by specific patterns of abnormal regional left ventricular systolic function. Regional contraction was quantitatively assessed from two-dimensional echocardiograms by an automated integrative analysis considering the time course of wall motion during the entire contraction sequence in 20 patients with chronic myocardial infarction, in 13 patients with impending myocardial infarction (less than 2 hr after the onset of symptoms), and in nine patients during transient myocardial ischemia. Wall motion abnormalities were detected in all patients by the integrative analysis. In contrast, the sensitivity for detecting wall motion abnormalities was 80% during chronic infarction, 77% during impending infarction, and 56% during transient ischemia if only end-diastolic and end-systolic frames were compared for assessment of overall regional systolic function. There were distinct differences in the time course of abnormal wall excursion between the three groups. Chronic infarction was characterized by a monophasic contraction pattern, with abnormal synergy in regional contractile events occurring predominantly during early systole. In contrast, transient ischemia caused predominantly mid-to-late systolic abnormal synergy followed by late systolic shortening corresponding to a polyphasic contraction pattern. During impending infarction, an intermediate temporal contraction pattern was present with both early and mesosystolic abnormal synergy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1997

Relaxation-systolic pressure relation. A load-independent assessment of left ventricular contractility.

This contribution reviews the regulation of left ventricular pressure (LVP) fall by load and relates this regulation to left ventricular contractility. Load regulation of LVP fall has to be distinguished from neurohumoral regulation, from effects induced by arterial reflected waves and from long-term load effects on contractility. The response of LVP fall to a moderate elevation of systolic LVP is highly variable. It depends on the ratio between the actual systolic pressure and peak isovolumetric pressure, defined as "relative load". Up to a relative load of 81% to 84%, LVP fall accelerates. Above this relative load, LVP fall decelerates. Depending on the level of relative load there is a wide variety of effects ranging from moderate acceleration of LVP fall to marked deceleration of LVP fall. Acceleration of LVP fall in response to a load elevation is associated with normal cardiac function, while slowing of LVP fall is associated with impaired cardiac function. Similar but opposite effects are observed with reductions of systolic LVP. Effects of changes in systolic LVP on time constant tau reveal a fair correlation with systolic elastance (Ees), peak dP/dtmax and regional fractional shortening (or ejection fraction). There is an excellent correlation with measured isovolumetric LVP, indicating that contraction-relaxation coupling is close when contractility is expressed in terms of peak isovolumetric pressure. Assessment of contractility with systolic LVP-relaxation relation is precise and load independent and can be performed with the sole use of a high-fidelity pressure gauge positioned in the left ventricular cavity.

Animals↗
PubMed1997

Hypertension and borderline isolated systolic hypertension increase risks of cardiovascular disease and mortality in male physicians.

BACKGROUND: The objective of this study was to examine whether definite hypertension and borderline isolated systolic hypertension predict subsequent cardiovascular disease and mortality. METHODS AND RESULTS: This was a prospective cohort study with a mean follow-up of 11.7 years. The subjects were a group of 18,682 apparently healthy US men, aged 40 to 84 years, participating in the Physicians' Health Study, a randomized trial of low-dose aspirin and beta-carotene. The main outcome measures were total cardiovascular disease, myocardial infarction, stroke, cardiovascular death, and all-cause mortality. Hypertension was associated with substantially increased risks of total cardiovascular disease (relative risk [RR] 1.92; 95% confidence interval [CI], 1.70 to 2.18), myocardial infarction (RR,1.78; 95% CI, 1.49 to 2.13), stroke (RR, 2.19; 95% CI, 1.78 to 2.69), and cardiovascular death (RR, 2.10; 95% CI, 1.68 to 2.63). Borderline isolated systolic hypertension was associated with significantly increased risks of cardiovascular disease (RR, 1.32; 95% CI, 1.09 to 1.59), stroke (RR, 1.42; 95% CI, 1.04 to 1.93), and cardiovascular death (RR, 1.56; 95% CI, 1.13 to 2.15), as well as a possible but non-significant increased risk of myocardial infarction (RR, 1.26; 95% CI, 0.95 to 1.67). Hypertension and borderline isolated systolic hypertension were associated with significantly increased risks of 41% and 22%, respectively, for all-cause mortality. CONCLUSIONS: Hypertension as well as borderline isolated systolic hypertension are associated with elevated risks of cardiovascular diseases, especially stroke and cardiovascular death. Hypertension is associated with an increased risk of myocardial infarction, and borderline isolated systolic hypertension predicts a possible but more modest increase in risk. These data add to the existing evidence that hypertension is a major cardiovascular risk factor and extend the findings to borderline isolated systolic hypertension.

Adult↗
PubMed1997

High homocysteine levels are independently related to isolated systolic hypertension in older adults.

BACKGROUND: The association between homocysteine and isolated systolic hypertension in older adults was evaluated using a case-control design, and the relationship between homocysteine and clinical or subclinical atherosclerosis was explored. METHODS AND RESULTS: Cases were 179 adults > or = 60 years with a systolic blood pressure of > or = 160 mm Hg and diastolic blood pressure < 90 mm Hg. One hundred seventy-one control subjects had the same criteria except systolic blood pressures were < 160 mm Hg. All had normal creatinine levels. Homocysteine levels were performed on fasting blood samples that had been stored at -70 degrees C. Atherosclerosis was defined as either a history of clinical disease, an internal carotid stenosis of > or = 40% by duplex scan, or an ankle/arm pressure ratio of < 0.9. The median homocysteine value was 11.5 micromol/L for cases and 9.9 for control subjects (P<.001). After control for potential confounders, homocysteine remained significantly associated with systolic hypertension (P=.019). For the hypertensive group, there was no apparent association between level of homocysteine and prevalence of atherosclerosis. However, among the normotensive group, the prevalence of atherosclerosis went from 22% in the lowest quintile of homocysteine values to 53% in the fifth quintile, with an odds ratio of 4.1 (fifth quintile in comparison to the first, P<.05). After adjustment for age, sex, systolic blood pressure, cholesterol, and smoking, this odds ratio increased to 6.4 (P<.01). CONCLUSIONS: Elevated levels of homocysteine may be related to the cause of isolated systolic hypertension in some individuals. In normotensive older adults, homocysteine appears to be an independent risk factor for atherosclerosis.

Aged↗
PubMed2006

Genetic determinants of systolic and pulse pressure in an intercross between normotensive inbred rats.

By continuous monitoring of abdominal aortic blood pressure via telemetry in conscious rats, we have observed that systolic, diastolic, and pulse pressures of male Brown-Norway rats were all significantly lower than that of male Wistar-Kyoto rats, despite the fact that all of the values in both strains were within normotensive ranges. Further analyses performed in 166 animals from the progeny of an F2 intercross between Brown-Norway and Wistar-Kyoto rats revealed that, despite a high correlation between systolic blood pressure and diastolic blood pressure, there was no correlation between pulse pressure and diastolic blood pressure, and the value of the correlation between systolic blood pressure and pulse pressure was lower than that of systolic blood pressure with diastolic blood pressure. Two major and highly significant (P<0.001) quantitative trait loci linked to pulse pressure were found on chromosome 4 (Pp1) and 16 (Pp2). Only suggestive quantitative trait loci were found for systolic blood pressure, but the strongest one (Sbp1) had the same peak and linkage probability profile as Pp1. Altogether, these data show that genetic determinants affecting pulse pressure in normotensive animals are either stronger or independent from the ones affecting systolic blood pressure and are of interest in light of evidence showing that pulse pressure is highly heritable in humans and that elevated pulse pressure is a predictor of cardiovascular risk.

Animals↗
PubMed2000

Possible locus on chromosome 18q influencing postural systolic blood pressure changes.

We conducted a genome-wide scan for quantitative trait loci influencing the systolic blood pressure, diastolic blood pressure, and pulse responses to a postural challenge in 498 white sibling-pairs from the Hypertension Genetic Epidemiology Network, a multicenter study of the genetic susceptibility to hypertension. All participants were hypertensive (systolic blood pressure >/=140 mm Hg, diastolic blood pressure >/=90 mm Hg, or on antihypertensive medications) with diagnosis before age 60. Blood pressure and pulse were measured by an oscillometric method after a 5-minute rest in a supine position and again immediately on standing. The genome scan included a total of 387 autosomal short-tandem-repeat polymorphisms typed by the National Heart, Lung, and Blood Institute Mammalian Genotyping Service at Marshfield. We used multipoint variance-components linkage analysis to identify possible quantitative trait loci influencing postural change phenotypes after adjusting for sex, age, and use of antihypertensive medications. There was suggestive evidence for linkage on chromosome 18q for the postural systolic blood pressure response (maximum logarithm of the odds score=2.6 at 80 centiMorgans). We also observed a maximum logarithm of the odds score of 1.9 for the systolic blood pressure response and 1.7 for the diastolic blood pressure response on chromosome 6p. The marker that demonstrated the strongest evidence for linkage for the systolic blood pressure response (D18S858) lies within 20 centiMorgans of a marker previously linked to rare familial orthostatic hypotensive syndrome. Our findings indicate that there may be 1 or more genes on chromosome 18q that regulate systolic blood pressure during the physiological recovery period after a postural stressor.

Age Distribution↗
PubMedDate not supplied

Systolic time intervals as possible predictors of pressure response to sustained beta-adrenergic blockade in arterial hypertension. A within-patient, placebo-controlled study.

Systolic time intervals (STI) were recorded at rest and during isometric exercise (IHG) in 20 hypertensive outpatients, WHO Stage 1 or 2. In a double-blind crossover study, slow-release metoprolol 200 mg once daily and matched placebo were given for 4 weeks each, at the end of a 2-week placebo washout. Blood pressure and STI were taken in the last day of washout and of either crossover period. Treatment decreased blood pressure and heart rate values at rest and on peak IHG; it didn't modify preejection period index (PEPI), left ventricular ejection time index (LVETI), and their ratio at rest, but decreased the ratio between diastolic blood pressure and PEPI (DBP/PEPI ratio) at rest and on peak IHG and lengthened the PEPI at peak IHG. Resting PEPI values on placebo treatment showed a negative correlation with systolic (r = -0.72) as well as diastolic (r = -0.80) pressure reduction on slow-release metoprolol as compared with placebo treatment. The PEP/LVET ratio at rest on placebo treatment showed a negative correlation with systolic (r = -0.78) as well as diastolic (r = -0.82) pressure reduction at rest on metoprolol compared with placebo treatment. Patients with a resting PEP/LVET ratio less than 0.43 showed a reduction in both systolic and diastolic pressure approximating or exceeding 20 mm Hg, whereas patients with a PEP/LVET ratio greater than 0.47 showed a decrease in systolic and diastolic blood pressure of less than 10 mm Hg. In patients with a PEP/LVET ratio of 0.43 to 0.47 (50% of the trial population), STI didn't show any correlation with the pressure response to beta-blockade. A positive correlation was found between the DBP/PEPI ratio at rest on placebo treatment and systolic (r = 0.56) as well as diastolic (r = 0.76) pressure reduction at rest on slow-release metoprolol compared with placebo treatment. Thus, STI appeared as promising predictors of the magnitude of blood pressure response to sustained beta-blocking therapy in mild-to-moderate essential hypertension, mostly in patients with a resting PEP/LVET ratio less then 0.43 or greater then 0.47.

Adult↗
PubMed2002

Isolated and borderline isolated systolic hypertension relative to long-term risk and type of stroke: a 20-year follow-up of the national health and nutrition survey.

BACKGROUND AND PURPOSE: Although the short-term risks of stroke and types of stroke associated with isolated systolic hypertension (ISH) and borderline isolated systolic hypertension (BISH) have been described, the long-term effects of these hypertensive conditions, particularly in younger individuals, are unclear. We performed this study to evaluate the long-term risks of stroke, type of stroke, and predictors of stroke associated with ISH and BISH and how this risk compares with that for persons with diastolic hypertension and normotension. METHODS: We used the 20-year follow-up data for 12 344 adults aged 25 to 74 years who participated in the First National Health and Nutrition Examination Survey Follow-Up Study to determine the aforementioned risks. Blood pressure (BP) measurements of the participants were obtained during baseline evaluation. ISH was defined as systolic BP >/=160 mm Hg and diastolic BP <90 mm Hg. BISH was defined as systolic BP between 140 and 159 mm Hg and diastolic BP <90 mm Hg. Diastolic hypertension was defined as a diastolic BP >/=90 mm Hg. Normotension was defined as systolic BP <140 mm Hg and diastolic BP <90 mm Hg. Incidence of stroke overall and incidence of ischemic stroke and intracerebral hemorrhage were determined from a review of hospital records and death certificates. Relative risk (RR) of stroke and stroke type in association with each hypertensive category was determined by Cox proportional hazards analysis after adjustment for potential confounding variables. RESULTS: Among the 12 344 participants, hypertension was categorized as ISH (n=493), BISH (n=1241), and diastolic hypertension (n=3954). Normotension was observed in 6656 persons. After adjustment for differences in age, sex, education, serum cholesterol level, body mass index, diabetes mellitus, and cigarette smoking, a significantly higher RR for all strokes was observed in participants with ISH (RR, 2.7; 95% CI, 2.0 to 3.4) and BISH (RR, 1.4; 95% CI, 1.1 to 1.8) than those with normotension. The risk was significantly higher for ischemic stroke or intracerebral hemorrhage in persons with ISH and BISH. Among the 1734 persons with either ISH or BISH, the risk of stroke was independently associated with older age, diabetes mellitus, and systolic BP >/=180 mm Hg. CONCLUSIONS: Increased risks for stroke, ischemic stroke, and intracerebral hemorrhage were observed in patients with BISH, similar to those associated with ISH and diastolic hypertension. Future clinical trials are required to evaluate the effect of antihypertensive treatment in younger patients with BISH and ISH.

Adult↗
PubMed1992

Predictive value of repeated systolic blood pressure measurements for stroke risk. The Zutphen Study.

BACKGROUND AND PURPOSE: The strength of the association between blood pressure and stroke incidence is dependent on the number of blood pressure measurements. Different summary variables of repeated blood pressure measurements taken during 10 years were evaluated in relation to the long-term risk of stroke in the Zutphen Study. METHODS: During the period 1960-1970 repeated blood pressure measures were taken yearly in 603 men aged 50-69 years in 1970 in the town of Zutphen, The Netherlands. The individual average systolic blood pressure between 1960 and 1970, the predicted systolic blood pressure for 1970 (based on regression of blood pressure readings on time), and the single observed systolic blood pressure in 1970 were used as systolic blood pressure estimates. Their strength in predicting the 15-year stroke incidence was assessed using Cox proportional hazards models. Adjustment was made for the confounding effects of age, cigarette smoking, and serum total cholesterol. RESULTS: The average systolic blood pressure between 1960 and 1970 was the strongest predictor of 15-year stroke incidence. The strength of the association was underestimated by 55% when a casual systolic blood pressure measurement was used instead of 11 yearly measurements. CONCLUSIONS: It can be concluded that a casual blood pressure measurement leads to a substantial underestimation of the long-term stroke risk of an individual.

Adult↗
PubMed2002

Development of predictive models for long-term cardiovascular risk associated with systolic and diastolic blood pressure.

Most existing risk prediction models have not considered the joint contribution of systolic and diastolic blood pressure to cardiovascular risk, and some suggest that there are thresholds below which further reductions of blood pressure yield no additional benefit. We developed multivariate risk prediction models that quantify the risk associated with both systolic and diastolic blood pressure and that can be used to infer the benefits of antihypertensive therapy in populations. Two large clinical trial cohorts, the Physicians' Health Study, composed of 22 071 males (mean age, 53.2 years; median follow-up, 13.0 years), and the Women's Health Study, composed of 39 876 females (mean age, 53.8 years; median follow-up, 6.2 years), were used to develop gender-specific predictive models via Cox regression. End points included myocardial infarction, stroke, coronary artery bypass, angioplasty, and cardiovascular death. Risk reduction estimates were derived by computing reductions associated with incremental lowering of systolic and diastolic blood pressures. In both populations, lower levels of blood pressure predicted lower event rates, with no evidence of a plateau or a J-shaped curve. In males, both systolic and diastolic blood pressures were significantly associated with events (P<0.001), whereas in females, only systolic blood pressure (P<0.001) predicted outcome after multivariate adjustment. Correction for measurement error in blood pressure increased risk estimates by approximately 50%. Differences in systolic blood pressure yielded greater relative risk reductions than did differences in diastolic blood pressure in a combined population of males and females. These predictive models may be useful for risk estimation associated with hypertension in similar populations and may also be used to infer the benefits of antihypertensive therapy.

Adult↗
PubMed2001

Late systolic wave on brachial artery blood flow velocity pattern in patients with coronary artery disease and its relation to vascular stiffness.

Duplex-Doppler study typically exhibits triphasic brachial artery blood flow velocity pattern in subjects classified as normal without clinically evident atherosclerotic complications, heart disease, hypertension, or diabetes mellitus. In this study, the authors described the late systolic wave on the brachial artery blood flow velocity pattern in patients with coronary artery disease and investigated the relation between late systolic wave and vascular stiffness. Blood flow profile and velocity of the brachial artery were determined noninvasively by ultrasound pulsed-Doppler technique under the guidance of a B-mode ultrasound image in 96 patients with coronary artery disease (CAD). The control group consisted of 23 healthy subjects with no or maximally 2 risk factors (only among age, cigarette smoking, obesity, and gender) for vascular disease. None of the patients and controls had clinical evidence of arterial disorders at upper extremities. In 32 patients (33%) with CAD, a late systolic wave was observed in the brachial artery Doppler study. On the other hand, no late systolic wave was observed in the healthy subjects. In addition, multivessel disease, hypertension, advanced age, diabetes, and smoking were significantly more frequent in patients with the late systolic wave. In conclusion, peripheral arterial abnormalities induced by vascular stiffness may produce alterations in regional wave reflections, and the normal triphasic pattern of the brachial artery blood flow may change by the appearance of the late systolic wave.

Adult↗
PubMed2000

Spurious systolic hypertension in youth.

Six young men diagnosed with systolic hypertension had normal carotid pressure wave contours, normal synthesized aortic pressure wave contours and normal diastolic and mean pressures in upper limb arteries. Elevated brachial systolic pressure was caused by a high narrow systolic peak of the pressure wave. This was attributed to amplification of the pressure wave between the ascending aorta and upper limb (radial and brachial) arteries that is associated with attainment of full body length and very distensible arteries. These young men were not truly hypertensive. Exaggeration of the upper limb systolic peak represented an extreme of the normal pressure wave pattern in youth, where amplification is greater than in childhood or in older subjects. This phenomenon accounts for the rapid increase in systolic pressure between the ages of 5 and 20 years, and the relative plateau in systolic pressure between the ages of 20 and 45 years that is seen in population studies.

Adolescent↗
PubMed1985

Augmented energy consumption during early systole as a mechanism of cyclical changes in high-energy phosphates in myocardium assessed by phosphorus nuclear magnetic resonance.

To evaluate the underlying mechanism of oscillatory changes in energy-related metabolites during a cardiac cycle, intramyocardial creatine phosphate (CP), inorganic phosphate (Pi), adenosine triphosphate (ATP), adenosine diphosphate (ADP) and pH were measured in isolated rat hearts by the phosphorus nuclear magnetic resonance spectrometry method gated by the left ventricular pressure. These were perfused with modified Krebs-Henseleit solution containing pyruvate. CP decreased at both early- and end-systole whereas Pi and ADP increased in these phases. Both ATP and intracellular pH decreased significantly at end-systole. The indices of the affinity for ATP hydrolysis [Pi]/[CP] and [ADP] [Pu]/[APT] increased at early-systole, indicating that a large consumption of high-energy phosphates occurred at early-systole. Furthermore, the cyclical changes in ATP, CP and Pi were augmented in the high contractile state induced by infusion of isoproterenol. These results strongly suggest that the cyclical changes in the energy-related metabolites during a cardiac cycle are caused mainly by an augmentation of energy consumption during early-systole and an insufficient energy supply during systole, probably due to the slow intracellular transport of CP.

Adenosine Diphosphate↗
PubMed1987

Evaluation of left ventricular contractility in hypertrophic cardiomyopathy from end-systolic pressure-volume relation.

To evaluate myocardial contractility in hypertrophic cardiomyopathy (HC), we obtained the end-systolic pressure-volume relation (ESPVR) and the end-systolic stress-volume relation (ESSVR) by changing loading conditions with Angiotensin II. The left ventricular (LV) stress-shortening relation was also analyzed in order to assess myocardial contractility. LV end-systolic pressure, end-systolic volume, end-systolic stress, and ejection fraction were obtained at rest and during Angiotensin II infusion with simultaneous recordings of pressure and volume in 9 patients with hypertrophic cardiomyopathy and 9 normal subjects (N). The slopes of ESPVR, Emax, showed no significant difference (HC: 3.1 +/- 2.3 vs N: 2.6 +/- 1.4 mmHg/ml, ns). The slopes of ESSVR were statistically similar (HC: 5.2 +/- 2.1 vs N: 6.0 +/- 2.8 g/cm2 ml, ns). The slopes of end-systolic stress-ejection fraction relation were also in the same range in both groups (HC: -0.09 +/- 0.05 vs N: -0.10 +/- 0.05, ns). From these two different analyses of LV contractility, we conclude that myocardial contractility is normal in hypertrophic cardiomyopathy and not supernormal, at both chamber and muscle levels. Considering the increased muscle mass in hypertrophic cardiomyopathy (HC: 134 +/- 46 vs N: 74 +/- 19 g/m2, p less than 0.01), the presence of increased numbers of contractile units does not result in enhanced overall chamber contractility.

Adult↗
PubMed1987

Quantitative analysis of regional wall motion in dogs in situ--characteristics of end-systolic pressure-length relation.

Regional wall motion was analyzed to deduce the muscle property unique to regional contractile states. End-systolic pressure length relations were evaluated under global changes in a contractile state, under selective intracoronary administration of inotropic agents to produce regional hypo- or hyper-kinesis, and before and after extension of size of the ischemia. Linearity of the end-systolic pressure-length relation was confirmed in each perturbation; however, the behavior of this relation with regard to changes in the slope and X-axis intercept differed among the three situations. When the contractile state was altered globally by intravenous administration of inotropic agents such as dobutamine and propranolol, the slope of the end-systolic pressure-length relation changed in a manner similar to that seen with the pressure-volume relation or stress-strain relation, with no significant changes in the X-axis intercept. Namely, the level of global cardiac function determined the slope of the end-systolic pressure length relation. When regional hypokinesis was produced pharmacologically by selective intracoronary infusion of lidocaine, the X-axis intercept moved rightward, depending on the degree of regional hypokinesis. Expansion in the size of the ischemic area also shifted the X-axis intercept rightward. The latter two phenomena suggested that the hypokinetic segments were stretched by the surrounding intact myocardium. Accordingly, end-systolic pressure-length relations provide useful information concerning the functional state of regional myocardium. The systolic properties of the regional myocardium rendered hypokinetic have to be quantified so as to include the total geometry of the heart.

Animals↗