Systemic Diastolic Pressure Research Articles

Systemic Arterial Pulsatility Index Predicts Adverse Outcomes in Cardiogenic Shock

Background Ventricular-arterial (VA) coupling has previously been shown to have physiologic importance in heart failure (HF). We hypothesized that a decreased systemic arterial pulsatility index (SAPi = [systemic systolic pressure - systemic diastolic pressure] / pulmonary capillary wedge pressure) would be associated with the adverse clinical outcomes in patients with systolic heart failure in cardiogenic shock (CS). Methods This was a retrospective study from a tertiary academic center. Patients with CS admitted to the coronary care unit (wedge pressure ≥15, cardiac index ≤2.2, and systolic blood pressure ≤90) were included. Using logistic regression analysis, we evaluated the association of SAPi to the outcomes of death or left ventricular assist device (LVAD). Results Among 119 patients with complete data (mean age 60.3 ± 14.7 years, 29% female), the median SAPi was 1.24 (IQR 0.91-1.68). Decreasing SAPi was strongly associated with outcome of death or LVAD [OR 0.52 (95% CI 0.29-0.95, chi square 4.54, p=0.03)]. Receiver operating characteristic curve analysis yielded an area under the curve (AUC) of 0.62 ± 0.06 (95% CI 0.490.73). Conclusion SAPi, an index of VA coupling, integrates pulse pressure and a proxy of left ventricular end-diastolic pressure. A decreased SAPi is strongly associated with adverse clinical outcomes in patients with CS and warrants consideration as a risk stratification tool.

Middle cerebral artery pressure changes following Pipeline flow diversion.

Objective Pipeline embolization devices (PED) are commonly used for endovascular treatment of cerebral aneurysms but changes in intracranial hemodynamics after PED deployment are poorly understood. Here, we assess middle cerebral artery (MCA) and systemic blood pressure before and after PED treatment. Methods Records of patients with cerebral aneurysms proximal to the internal carotid artery terminus treated with PED at our institution between 2015 and 2017 were retrospectively reviewed. Patients were included if ipsilateral MCA pressure measurements were available. Ipsilateral MCA pressure was transduced via the microcatheter before and after PED deployment. Systemic arterial blood pressure was also simultaneously recorded. MCA, systemic blood pressure, and ratios of MCA to systemic blood pressure values were compared before and after treatment among the study cohort using the two-sample paired Student t test. Results Fourteen patients were included. Mean age was 54 years. Among the entire cohort, the ratio of MCA to systemic systolic and mean blood pressure were significantly higher after treatment (respectively 0.76 vs. 0.69, p = 0.01, and 0.94 vs. 0.89, p = 0.03), and the ratio of MCA to systemic diastolic pressures showed an increasing trend (1.08 vs. 1.03, p = 0.09). The percentage of ratio increase was independent of aneurysm size ( r = -0.24, p = 0.42 for systolic ratio; r = -0.09, p = 0.74 for diastolic ratio; r = -0.09; p = 0.76 for mean ratio, respectively). Conclusions Following PED deployment, the ratio of ipsilateral MCA to systemic systolic and mean blood pressure increased. These pressure changes should be further evaluated in a larger sample size.

Systemic diastolic pressure at induction: a potential new metric associated with failed extubation by 24h following cardiopulmonary bypass

Systemic diastolic pressure at induction: a potential new metric associated with failed extubation by 24h following cardiopulmonary bypass

Threatening Inferior Limb Ischemia: When to Consider Fasciotomy and What Principles to Apply?

Inferior limb compartmental syndrome (CS) gathers a constellation of symptoms that traditionally refers to pathologically increased intramuscular and surrounding tissue pressure generally contained in nonexpansile leg spaces. It associates oftentimes reperfusion or traumatic injury. Intrinsic rigidity of these leg and foot closed compartments may enhance critical pressure risings with deleterious effects on specific vascular and nervous supply, with two main presentations: acute versus chronic display. For these situations, early fasciotomy plays the major role of releasing specific compartment hypertension and prevents deleterious tissue necrosis. Intervention is effective only if required upon precise indications (measured tissue pressure within 20 to 30 mm Hg of systemic diastolic pressure) and performed correctly in a timely fashioned approach. Any failure or delay in recognizing CS inevitably leads to adverse outcomes and jeopardy for secondary limb loss. When judiciously applied during or soon after limb-salvage revascularization technically successful fasciotomy may represent a major contributor in limb preservation. It accounts for a well-defined therapeutic proceeding available for any conscientious and well-briefed interventionist.

First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms

Endovascular stent graft repair of abdominal aortic aneurysms (AAAs) prevents rupture by excluding the aneurysm sac from systemic arterial pressure. Current surveillance protocols after endovascular aneurysm repair (EVAR) follow secondary markers of sac pressurization, namely, endoleak and sac enlargement. We report the first clinical experience with the use of a permanently implantable, ultrasound-activated remote pressure transducer to measure intrasac pressure after EVAR. Over 7 months, 14 patients underwent EVAR of an infrarenal abdominal aortic aneurysm with implantation of an ultrasound-activated remote pressure transducer fixed to the outside of the stent graft and exposed to the excluded aortic sac. Twelve patients received modular bifurcated stent grafts, and 2 patients received aortouniiliac devices. Intrasac pressures were measured directly with an intravascular catheter and by the remote sensor at stent-graft deployment. Follow-up sac pressures were measured with a remote sensor and correlated with systemic arterial pressure at every follow-up visit. Mean follow-up was 2.6 +/-1.9 months. Excellent concordance was found between catheter-derived and transducer-derived intrasac pressssure intraoperatively. Pulsatile waveforms were seen in all functioning transducers at each evaluation interval. One implant ceased to function at 2 months of follow-up. In 1 patient a type I endoleak was diagnosed on 1-month computed tomography (CT) scans; 3 type II endoleaks were observed. Those patients with complete exclusion of the aneurysm on CT scans had a significant difference in systemic and sac systolic pressures initially (P <.001) and at 1 month (P <.001). Initial sac diastolic pressures were higher than systemic diastolic pressures (P <.001). The ratio of systemic to sac systolic pressure increased over time in those patients with complete aneurysm exclusion ( P <.001). Four of 6 patients with no endoleak and greater than 1-month follow-up had diminution of sac systolic pressure to 40 mm Hg or less by 3 months. This is the first report of a totally implantable chronic pressure transducer to monitor the results of EVAR in human beings. Aneurysm exclusion leads to gradual diminution of sac pressure over several months. Additional clinical follow-up will be necessary to determine whether aneurysm sac pressure monitoring can replace CT in the long-term surveillance of patients after EVAR.

Intra-aneurysmal pressure after incomplete endovascular exclusion

Purpose: An endoleak results from the incomplete endovascular exclusion of an aneurysm. We developed an experimental model to analyze hemodynamic changes within the aneurysm sac in the presence of an endoleak, with and without a simulated open collateral branch. Methods: With a latex aneurysm model connected to a pulsatile pump, pressures were measured simultaneously within the system (systemic pressure) and the aneurysm sac (intrasac pressure). The experiments were performed without endoleak (control group) and after creating a 3.5-mm (group 1), 4.5-mm (group 2), and 6-mm (group 3) diameter orifice in the endograft, simulating an endoleak. Pressures were also registered with and without a patent aneurysm side branch. Results: In each endoleak group, the intrasac diastolic pressure (DP) and mean pressure (MP) were significantly higher than the systemic DP and MP (P =.01, P =.006, and P =.001, respectively), although the pressure curve was damped. The presence of an open side branch significantly reduced the intrasac DP and MP. Conclusion: In this model, intrasac pressures were significantly higher than systemic pressures in the presence of all endoleaks, even the smallest ones. Intrasac pressures higher than systemic pressure may pose a high risk for aneurysm rupture. Although patent side branches significantly reduce these pressures, the aggressive management of an endoleak should be pursued. (J Vasc Surg 2001;33:909-14.)

Endoleakage after stent-graft treatment of abdominal aneurysm: Implications on pressure and imaging—an in vitro study

Background: Endoleakage is a fairly common problem after endovascular repair of abdominal aortic aneurysm and may prevent successful exclusion of the aneurysm. The consequences of endoleakage in terms of pressure in the aneurysmal sac are not exactly known. Moreover, the diagnosis of endoleakage is a problem because visualization of endoleaks can be difficult. Method: With an ex vivo model of circulation with an artificial aneurysm managed by means of a tube graft, studies were performed to evaluate precisely known diameters of endoleaks with both imaging techniques (computed tomography and digital subtraction angiography) and pressure measurements of the aneurysmal sac. The experiments were performed without endoleak (controls) and with 1.231-French (0.410 mm), 3-French (1 mm), and 7-French (2.33 mm) endoleaks. Pressure and imaging were evaluated in the absence and presence of a simulated open lumbar artery. The pressure in the prosthesis and in the aneurysmal sac were recorded simultaneously. Digital subtraction angiography with and without a Lucite acrylic plate, computed tomographic angiography, and delayed computed tomographic angiography were performed. For the first experiments, the aneurysmal sac was filled with starch solution. All tests were repeated with fresh thrombus in the aneurysmal sac. Results: Each endoleak was associated with a diastolic pressure in the aneurysmal sac that was identical to diastolic systemic pressure, although the pressure curve was damped. At digital subtraction angiography without a Lucite acrylic plate, the 1.231-French (0.410 mm) endoleak was visualized without an open lumbar artery. When a Lucite acrylic plate was added, the endoleak was not visible until a lumbar artery was opened. In the presence of thrombus within the aneurysmal sac, all endoleaks were not visualized at digital subtraction angiography. At computed tomographic angiography, all endoleaks were not visualized in the absence of a thrombus mass in the aneurysmal sac. In the presence of thrombus within the aneurysmal sac, the 1.231-French (0.410 mm) endoleak became visible after opening of a simulated lumbar artery. At delayed computed tomographic angiography, all endoleaks were visualized without and with thrombus. Conclusion: Every endoleak, even a very small one, caused pressure greater than systemic diastolic pressure within the aneurysmal sac. However, small endoleaks were not visualized with digital subtraction angiography and computed tomographic angiography, whereas all endoleaks were visualized with a delayed computed tomographic angiography protocol. We believe that follow-up examinations after stent graft placement for aortic aneurysms should focus on pressure measurements, but until this is clinically feasible, delayed computed tomographic angiography should be performed. (J Vasc Surg 1998;28:234-41.)

Accurate Noninvasive Estimation of Left Ventricular End-Diastolic Pressure: Comparison with Catheterization

We evaluated the accuracy of a new Doppler-based method using the mitral regurgitant velocity at the time of aortic valve opening for the noninvasive estimation of left ventricular end-diastolic pressure. Sixty unselected patients were studied immediately before routine catheterization. Invasive left ventricular end-diastolic pressure was obtained using a fluid-filled pig-tail catheter. Noninvasive estimation of left ventricular pressure at aortic valve opening was taken as systemic diastolic pressure using an automated cuff. Noninvasive left ventricular end-diastolic pressure was calculated as diastolic blood pressure - 4 × (mitral regurgitant velocity at aortic opening) 2 . Those making noninvasive determinations were blinded to catheterization results. An adequate mitral regurgitant Doppler recording was obtained in 24 patients (40%). In patients with a left ventricular end-diastolic pressure greater than 15 mm Hg the yield was 65%. Left ventricular end-diastolic pressures ranged from 4 mm Hg to 30 mm Hg. Bland and Altman analysis revealed no systematic bias and close agreement was found, with individual discrepancies not exceeding 5 mm Hg. (J Am Soc Echocardiogr 1998;11:126–31.)

Autogenous cardiac assist with chronic descending thoracic aortomyoplasty

Alternative surgical treatments to orthotopic cardiac transplantation are needed for patients with heart failure. We hypothesized that descending thoracic aortomyoplasty with conditioned (fatigue-resistant) latissimus dorsi muscle could provide diastolic augmentation that would improve left ventricular function. Six mongrel dogs were studied. The left latissimus dorsi muscle was wrapped clockwise around the descending thoracic aorta. Left ventricular volume was measured with a conductance catheter. Aortic and left ventricular pressures were measured with a micromanometer The following were measured after descending thoracic aortomyoplasty at baseline and with the descending thoracic aortomyoptasty stimulated 1:1 with the heart rate: stroke work, stroke volume, left ventricular peak pressure, maximum rate of increase of left ventricular pressure, diastolic relaxation time constant, peak rate of pressure decay, left ventricular end-diastolic pressure, endocardial viability ratio, mean diastolic aortic pressure, peak diastolic aortic pressure, and time-averaged aortic diastolic velocity. Before data collection, the latissimus dorsi was stimulated (5 pulses delivered at 33 Hz at a rate of 28 per minute for 4 weeks) with burst stimulation to induce fatigue resistance. Results (expressed as the mean ± the standard error of the mean) showed significant improvement in the indices of ventricular contractility (maximum rate of increase of left ventricular pressure, 1,217 ± 83 to 1,414 ± 91 mm Hg/s) and diastolc relaxation mechanics (peak rate of pressure decay, 1,152 ± 92 to 1,282 ± 79 mm Hg/s; diastolic relaxation time constant 43 ± 2 to 38 ± 2 ms). Significant differences were noted with stimulation at 1:1 in the endocardial viability ratio (0.90 ± 0.05 to 1.14 ± 0.04), an index of myocaidial oxygen supply. Systemic diastolic pressures (peak diastolic aortic pressure, 95 ± 6 to 107 ± 5 mm Hg; mean diastolic aortic pressure, 92 ± 6 to 102 ± 6 mm Hg) and the tune-averaged aortic diastolic velocity (1.5 ± 0.6 to 3.3 ± 1.0 m/s) increased significantly. We conclude that descending thoracic aortomyoplasty stimulation with conditioned latissimus dorsi muscle can improve indkes of ventricular contractility, diastolic relaxation mechanics, diastolic pressures, and diastolic aortic velocity in the nonfailed canine heart. Farther studies with the chronic failed heart model are required.

Intraoperative measurements of cerebral haemodynamics during ductus arteriosus ligation in preterm infants

Intraoperative Doppler sonographic examinations were carried out on seven preterm neonates to measure cerebral blood flow velocity changes in the anterior cerebral arteries during ductus arteriosus ligation. Age at surgery was 12 +/- 6 days. Continuous recordings during the operative procedure showed a rapid increase in diastolic blood pressure (P less than 0.01), whereas systolic blood pressure was not significantly higher compared with pre-occlusion values. In the anterior cerebral arteries, ductal closure led to a decrease in resistance index of Pourcelot (mean = 1.02 +/- 0.08 vs 0.65 +/- 0.07 (P less than 0.001)) and to an increase in area under the velocity curve (mean = 3.64 +/- 0.38 vs 8.16 +/- 1.07 (P less than 0.001)). These changes were associated with a corresponding increase of the end diastolic flow velocity (P less than 0.001) but no change in the peak systolic velocity. The heart rate did not change significantly during ductal closure. TcPO2, TcPCO2 remained normal during the study period. These data indicate that changes in cerebral blood flow velocity during surgical ligation are principally determined by changes in systemic diastolic pressure. Systolic blood pressure and peak systolic flow velocity remain unchanged or slightly higher than preligation values, thereby restoring normal cerebral blood flow velocity pattern without increasing the stress on the wall of cerebral vessels and thus the risk of peri-intraventricular haemorrhage.

Estimation of Regurgitant Volume and Orifice in Aortic Regurgitation Combining CW Doppler and Parameter Estimation in a Windkessel Like Model

A method for noninvasive estimation of regurgitant orifice and volume in aortic regurgitation is proposed. The method was tested in anesthetized open-chested pigs. It can be used with noninvasive measurement of regurgitant jet velocity using continuous-wave ultrasound Doppler measurements together with cuff measurements of systolic and diastolic systemic pressure in the arm. These measurements are then used for parameter estimation in a Windkessel-like model which includes the regurgitant orifice as a parameter. The aortic volume compliance and the peripheral resistance are also included as parameters and estimated in the same process. Electromagnetic flow measurements in the ascending aorta and pulmonary artery are used for control. The correlation obtained between regurgitant volume derived from parameter estimation and from electromagnetic flow measurements is 0.95 over a range from 2.1 to 17.8 mL. >

Estimation of regurgitant volume and orifice in aortic regurgitation combining CW Doppler and parameter estimation in a Windkessel-like model

A method for noninvasive estimation of regurgitant orifice and volume in aortic regurgitation is proposed and tested in anesthetized open chested pigs. The method can be used with noninvasive measurement of regurgitant jet velocity with continuous wave ultrasound Doppler measurements together with cuff measurements of systolic and diastolic systemic pressure in the arm. These measurements are then used for parameter estimation in a Windkessel-like model which include the regurgitant orifice as a parameter. The aortic volume compliance and the peripheral resistance are also included as parameters measurements in the open chest pigs are used. Electromagnetic flow measurements in the ascending aorta and pulmonary artery are used for control, and a correlation between regurgitant volume obtained from parameter estimation and electromagnetic flow measurements of 0.95 over a range from 2.1 to 17.8 mL is obtained.

Comparison of the Effects of Nifedipine and Nitroglycerin on Hemodynamic Determinants of Myocardial Oxygen Consumption and Supply During Exertional Angina

To investigate the antianginal action of nitroglycerin and nifedipine, systemic and right heart pressures, cardiac output, oxygen consumption, and radionuclide left ventricular ejection fraction and volume were measured in 14 men with stable effort angina and a positive exercise electrocardiogram. Exercise tests were performed on a semiupright bicycle ergometer on no therapy and after intravenous nitroglycerin and sublingual nifedipine, which lowered mean arterial pressure by 20 mm Hg. Exercise tolerance improved from 50 +/- 4 to 61 +/- 5 W on nifedipine and to 79 +/- 4 W on nitroglycerin (p less than 0.01, nitroglycerin vs. nifedipine). At submaximal workloads, both drugs decreased arterial pressure and ventricular volumes, but heart rate was higher on nifedipine. At peak exercise on nitroglycerin (79 W), oxygen consumption, cardiac index, heart rate, and rate-pressure product were significantly increased over peak control and nifedipine values, while systolic pressure and end-diastolic volume were unchanged. Nitroglycerin reduced pulmonary wedge pressure more and systemic diastolic pressure less than nifedipine, so the coronary perfusion gradient was reduced by nifedipine and maintained by nitroglycerin. Also, there was less angina and ST-segment depression after nitroglycerin compared to control or nifedipine, and the left ventricular diastolic pressure-volume relationship was improved only by nitroglycerin. This suggests that the action of nitroglycerin in reducing ischemia is not only due to reduced myocardial oxygen demand, but that myocardial oxygen delivery may also be increased.

Effects of diltiazem, a calcium channel inhibitor, in retarding cellular damage produced during early myocardial ischemia in pigs: A morphometric and ultrastructural analysis

A protective effect of intravenous diltiazem pretreatment on transmural histologic damage in ischemic hearts of 30 pigs was determined morphometrically. The pig hearts were rendered ischemic by ligation of the distal left anterior descending coronary artery for 20, 40 and 120 minutes in separate experiments. Heart rate, left ventricular systolic pressure and systemic diastolic pressure decreased slightly during 40 minutes of occlusion, and then recovered to control levels. However, there were no significant differences between control and diltiazem-treated groups. Blood flow, measured by the microsphere technique, was uniformly absent in the ischemic areas in both control and diltiazem-treated hearts. In the few cell layers immediately beneath the endocardium and epicardium, little cellular damage was observed in either group regardless of the duration of ischemia. In the subendocardial, mid-myocardial and subepicardial layers, less cellular damage was detected after all periods of ischemia in hearts exposed to diltiazem in comparison with that observed in control hearts. However, even in the drug-treated hearts, after 2 hours of occlusion, the cells remained severely injured. The protective effect of diltiazem on the cellular integrity in the ischemic myocardial regions appears to be independent of blood flow and may be a reflection of a direct effect of diltiazem on myocytes. The precise mechanism is unresolved. Nevertheless, in the ischemic heart without a significant collateral circulation, pretreatment with the calcium channel blocking drug, diltiazem, results in a delayed onset of cellular damage after acute coronary artery ligation and less cellular damage at ischemic periods up to 40 minutes' duration.

The effect of patent ductus arteriosus on flow velocity in the anterior cerebral arteries: Ductal steal in the premature newborn infant

Marked changes in blood flow velocity in the anterior cerebral arteries, measured by a Doppler technique, have been related to PDA in premature infants. Thus, 55 premature infants of birth weight less than 2,000 gm were studied. Ten developed PDA between days three and ten of life. A sharp decrease in diastolic flow velocity and an increase in pulse amplitude in the ACA was observed with the occurrence of PDA. Return of these values to normal occurred promptly following closure of the lesion. These changes in flow velocity and pulse amplitude in the ACA appear to be determined principally by changes in systemic diastolic pressure which accompany PDA. There was no consistent relationship between the changes in flow velocity and arterial PCO2 values. These data suggest that PDA may be involved in the genesis of ischemic and hemorrhagic cerebral injury in the premature newborn infant. Thus, the decrease in flow velocity appears to represent a "steal" of blood from the cerebral arteries, analogous to other documented steal phenomena observed in older patients. Major fluctuations of blood flow velocity in the ACA, with opening and closure of the PDA, and the increase in amplitude of each pulse with PDA may, in the presence of disturbed autoregulation, cause rupture of the capillaries of the germinal matrix and thus, IVH.

Ophtalmodynamographie pneumatique au biomicroscope*

One hundred volunteers were examined with a new pneumatic dynamometer which permits the use of the slit lamp and the Hruby lens, this is a noncorneal-contact instrument indicating the relationship between diastolic systemic pressure and diastolic ophthalmic pressure; in the latter case, the pressures in the two eyes are compared.

Hemodynamic response of the pancreas to synthetic chicken VIP in dogs.

The effects of synthetic chicken VIP (an octacosapeptide corresponding to the entire sequence of chicken VIP) on pancreatic blood flow and on systemic arterial pressure was examined in dogs. The relationship between pancreatic blood flow and systemic arterial pressure in response to synthetic chicken VIP was also investigated. Pancreatic blood flow increased promptly and significantly with exogenous synthetic chicken VIP. Synthetic chicken VIP administered in graded doses resulted in dose-dependent increases in both the peak rate of the pancreatic blood flow and the duration of the response of the pancreatic blood flow. Graded doses of synthetic chicken VIP also elicited both a graded increase in the systemic systolic pressure and a decrease in the systemic diastolic pressure. Therefore, synthetic chicken VIP given in graded doses resulted in a dose-dependent augmentation of the maximum pulse pressure. Pancreatic blood flow increased despite a fall in the systemic arterial pressure in response to synthetic chicken VIP. This increase in blood flow lasted significantly longer than the changes in the systemic arterial pressure. It was clarified in this study that synthetic chicken VIP has a biological effect on both the pancreatic blood flow and the systemic arterial pressure. The results of our experiments also suggest that synthetic chicken VIP itself may directly induced vasodilatation of the local vessels in the pancreas.

Sustained haemodynamic action of nitroglycerin ointment.

Intravenous vasodilators have been shown to improve the haemodynamic status of patients in congestive heart failure. However, neither intravenous nor sublingual preparations are suitable for chronic administration or use in ambulatory patients. In this study, nitroglycerin ointment bas administered to 11 patients in congestive heart failure. Mean pulmonary wedge and arterial pressures, as well as systemic blood pressures and heart rate were then monitored for 2 to 5 hours and compared with baseline values. Pulmonary wedge and arterial pressures, as well as systemic systolic arterial pressure, decreased significantly at 15 minutes after application and remained depressed for up to 5 hours. Systemic diastolic pressures fell significantly at 30 minutes and also remained significantly reduced for up to 5 hours. Thus, nitroglycerin ointment may be suitable for chronic vasodilator therapy of congestive heart failure.

Idiopathic left ventricular hypertrophy: A hemodynamic reappraisal

Left ventricular end-systolic and end-diastolic volumes were measured by a thermodilution technic in four patients with idiopathic left ventricular hypertrophy. Two patients had no outflow tract obstruction at rest and the ventricular end-diastolic volumes were 90 and 107 ml. per M 2. Two patients with idiopathic hypertrophic subaortic stenosis (IHSAS) with large gradients, had end-diastolic volumes of 69 and 67 ml. per M 2. The lower limit of normal for this value in our laboratory is 90 ml. per M 2. The low end-diastolic volumes in the two patients with IHSAS were associated with ventricular end-diastolic pressures of 18 and 20 mm. Hg, indicating that the diastolic compliance of the left ventricle was severely reduced. This low compliance produced a high mean left atrial pressure and a low stroke volume, due to inadequate ventricular filling. It is postulated that in some cases of IHSAS, such handicaps may be as important as outflow tract obstruction. When methoxamine was administered to two patients with IHSAS, the systemic pressure rose and the outflow gradient was lessened in both. However, in one case the ventricular enddiastolic volume rose from 69 to 79 ml. per M 2., and in the other it fell from 90 to 59 ml. per M 2. Based on our data, and other studies from the literature, it is suggested that systemic diastolic pressure is an important determinant of the outflow gradient in IHSAS. A rise in systemic diastolic pressure may reduce, or even nullify, the effects of either a reduced ventricular systolic volume or positive inotropic stimulation, both of which have been shown to increase outflow obstruction. It is proposed that the gradient in IHSAS depends on a complex interplay of variables, some tending to increase the gradient, and some tending to decrease it. It may thus be difficult to predict the effect of any agent or maneuver in a given patient with IHSAS.