Diastolic Pressure Time Index Research Articles

Myocardial Oxygen Supply-Demand Ratio: A Validation of Peripherally vs Centrally Determined Values

We sought to validate that the supply-demand ratio for myocardial oxygen could be accurately measured from tracings of peripheral as well as central arterial pressure. This ratio was the ratio of the diastolic pressure-time-index (DPTI) over the systolic pressure-time index (SPTI). Sixteen patients had the peripheral DPTI/SPTI determined at cardiac catheterization by the following two different methods: (1) P1, using the mean diastolic and systolic peripheral arterial pressure and the ratio of the duration of diastole and systole; and (2) P2, where the peak systolic and diastolic peripheral arterial pressures are used, eliminating the need for planimetric data. The results of P1 and P2 correlated closely with the central value (r = 0.96 and 0.92, respectively). We conclude that DPTI/SPTI can reliably be measured from a tracing of peripheral arterial pressure, enabling reliable continuous monitoring of this ratio. We sought to validate that the supply-demand ratio for myocardial oxygen could be accurately measured from tracings of peripheral as well as central arterial pressure. This ratio was the ratio of the diastolic pressure-time-index (DPTI) over the systolic pressure-time index (SPTI). Sixteen patients had the peripheral DPTI/SPTI determined at cardiac catheterization by the following two different methods: (1) P1, using the mean diastolic and systolic peripheral arterial pressure and the ratio of the duration of diastole and systole; and (2) P2, where the peak systolic and diastolic peripheral arterial pressures are used, eliminating the need for planimetric data. The results of P1 and P2 correlated closely with the central value (r = 0.96 and 0.92, respectively). We conclude that DPTI/SPTI can reliably be measured from a tracing of peripheral arterial pressure, enabling reliable continuous monitoring of this ratio.

Total and regional myocardial blood flow in aortic regurgitation

Total, phasic, and regional flow were studied in 12 open-chest dogs with aortic regurgitation. An adjustable catheter device was used to produce aortic regurgitation. Four differently labeled 7 to 9μ microspheres were injected into the left atrium during control, mild (5 to 25 per cent), moderate (25 to 50 per cent), and severe (50 to 80 per cent) regurgitation. Aortic regurgitation (AR) and the ratio of diastolic coronary blood flow to systolic coronary blood flow ( DIAS SYS RATIO) were measured from the electromagnetic flow tracings. The simultaneous left ventricular and aortic pressures were used to calculate DPTI SPTI (diastolic pressure time index to systolic time index). Myocardial flow, flow to major subgroups, and endocardial/epicardial ratios were determined from radioisotope analysis of the left ventricle. Mean absolute control values and mean changes of key variables from control were: 3 Control Mild AR Mod AR Severe AR Heart rate (beats/min.) 163.42 −5.00 −4.83 ∗ −8.56 DPTI SPTI 1.18 −0.12 ∗ −0.24 ∗ −0.56 ∗ Dias/Sys ratio 4.23 −0.28 −1.64 ∗ −3.31 ∗ Myo. flow (ml./100g./min.) 99.90 −5.63 11.18 21.63 Endocardium (ml./100 g./min.) 97.27 −5.28 10.26 7.39 Epicardium (ml./100 g./min.) 100.15 −7.38 7.88 21.58 ENDO EPI ratio 0.99 0.01 0.01 −0.11 ∗ Denotes significant change from control state (P = 0.05). The phasic coronary blood flow results in this study are similar to those reported in chronic, intact anesthetized dogs; when the degree of aortic regurgitation increased, there was a significant decrease in diastolic coronary blood flow with an increase in systolic coronary blood flow. Not previously reported are the changes in the distribution of myocardial perfusion. Total myocardial flow increased slightly. There were minimal changes in blood flow to the endocardium which resulted in a slight decrease in the ENDO EPI ratio and a decrease in the per cent of flow to the endocardium. These results indicate that, although acute aortic regurgitation produces significant changes in phasic coronary flow, there are much smaller effects on total and regional myocardial blood flow.

Cardiac function during induction and early anesthesia with methoxyflurane. An evaluation using systolic time intervals and pressure time indices.

In addition to the standard monitoring of heart rate and blood pressure, the Systolic Time Intervals were used to evaluate cardiac performance, and the Pressure Time Indices (tension time index = TTI; diastolic pressure time index = DPTI) were used to estimate myocardial oxygen balance. Twelve patients with known heart disease were studied during induction with thiopental, intubation, and early anesthesia with methoxyflurane. Cardiac performance diminished after thiopental; and during methoxyflurane it was reflected in increases in pre-ejection period (PEP) and the ratio PEP/LVET. Intubation resulted in a hyperactive state of the heart, as shown by maximal decreases in PEP and PEP/LVET. Myocardial oxygen balance--estimated from the supply/demand ratio (DPTI/TTI)--was impaired after thiopental. After intubation, DPTI/TTI decreased to its lowest value due to an excess of myocardial oxygen demand (TTI) over myocardial oxygen supply (DPTI), signifying a transitory underperfusion of the subendocardium. During methoxyflurane the oxygen balance was gradually restored towards control value. The Systolic Time Intervals and the Pressure Time Indices provided valuable information on cardiac function not available from standard monitoring alone.

Examination of the validity of the DPTI as an estimate of myocardial oxygen supply with special reference to the DPTI/TTI ratio.

The validity of the diastolic pressure time index (DPTI) as an estimate of myocardial O2 supply and tension time index (TTI) as an estimate of O2 demand has been examined in 10 closed-chest anesthetized dogs. We analyzed 158 steady states including maximal variation of hemodynamics and O2 consumption. For each steady state 23 hemodynamic variables were calculated. Myocardial blood flow (MBF) was directly measured in the coronary sinus with a differential pressure catheter. Oxygen consumption (MVO2) was varied by application of catecholamines, atropine, negative and positive inotropic drugs and hypo- and hypervolemia. There was a close relationship between direct measurements of O2 supply and O2 demand over a wide range of testing (r=0.93), but there was no significant correlation between the ratio of DPTI/TTI and the ratio of O2 supply/O2 demand (directly measured). With intact metabolic regulation of coronary blood flow there is no close correlation of mean diastolic aortic pressure to coronary blood flow (r=0.45) over the entire tested range, which is one reason why the DPTI does not show a correlation to the direct measurement of O2 supply (r=0.34). The tension time index bears a close relationship to myocardial oxygen consumption only under normal and moderate stimulation of inotropism (r=0.96), but there is no significant correlation under high positive inotropic stimulation (r=0.39). Our findings indicate that the ratio of DPTI/TTI should be interpreted with great care if it is generally used as an indicator of the adequacy of myocardial O2 supply.

Monitoring myocardial performance after open heart surgery by calculation of diastolic and systolic pressure time index (author's transl)

In order to determine the incidence of subendocardial ischemia after open heart surgery, subendocardial blood flow was monitored in 171 patients subjected to mitral and/or aortic valve replacement or coronary revascularization by on-line calculation of Diastolic (DPTI) and Systolic Pressure Time Index (TTI). Body hypothermia with an esophageal temperature of 25 degrees C and magnesium-aspartate-procaine cardioplegia were applied for myocardial protection. Ten patients developed low cardiac output state with two early deaths. In the two patients with fatal low cardiac output DPTI/TTI remained below 0.8. In the remaining 8 patients DPTI/TTI rose to 1.4 after a mean recovery time of 36 hours. In 161 patients (94%) no low cardiac output state evolved and DPTI/TTI rose to 1.3 within 60 min. after termination of cardiopulmonary bypass. Our results indicate that body hypothermia of 25 degrees C combined with magnesium-aspartate-procaine cardioplegia can reduce the incidence of subendocardial ischemia, but does not prevent this complication completely after anoxic times beyond 60-70 minutes.

Haemodynamic effects on the myocardial blood flow supply/oxygen demand ratio in pacing induced angina pectoris.

Angina pectoris results from an imbalance between oxygen supply and demand in the subendocardium. The haemodynamic effects contributing to this imbalance have been studied in 10 patients with coronary artery disease. Myocardial oxygen demand was estimated from the tension time index (TTI), potential subendocardial flow from a diastolic pressure time index (DPTI), and the oxygen supply/demand ratio from (DPTI/TTI. With progressively increasing pacing rates up until induction of angina, no significant change in TTI was found whereas a significant fall in DPTI and DPTI/TTI occurred (P less than 0.001). During pacing runs with induction of angina DPTI/TTI reached a minimum value 5 s before,and at the onset of angina. No such relationship was seen for TTI or DPTI alone. A significant rise in LVEDP (P less than 0.05) and fall in dP/dt min (P less than 0.01) occurred at angina both contributing to a further reduction in DPTI and DPTI/TTI. Changes in DPTI/TTI may then reflect changes in the myocardial blood flow supply/oxygen demand ratio in the presence of coronary artery disease and haemodynamic changes before and at the induction of angina lead to a further reduction of this ratio.

Alterations in total and regional myocardial blood flow during acute rejection of orthotopic canine cardiac allografts

Using radioactive microspheres, we studied the quantitative and sequential distribution of myocardial blood flow during acute rejection of cardiac orthotopic allografts in 15 nonimmunosuppressed dogs. During rejection mean cardiac output per kilogram decreased 49 percent from control, stroke volume per kilogram decreased 40 percent, total left ventricular flow decreased 43 percent, and the subendocardial/subepicardial flow ratio (I/O) of the left ventricular free wall decreased 21 percent. Relative subendocardial hypoperfusion occurred despite an increase in the ratio of left ventricle subendocardial supply (diastolic pressure-time index) to demand (tension-time index). The data indicate that total left ventricular flow decreases severely and selective left ventricular subendocardial ischemia develops very early during acute cardiac rejection.

Subendocardial ischaemia in patients with discrete subvalvar aortic stenosis.

The evidence for subendocardial ischaemia was studied in 12 patients with discrete subvalvar aortic stenosis. Symptomatology, electrocardiographic criteria, and pressure difference across the left ventricular outflow tract were compared with the subendocardial flow index (diastolic pressure time index systolic pressure time index). All symptomatic patients had a large pressure difference and abnormal index, but 4 asymptomatic patients had pressure differences greater than 60 mmHg and a low index. One of these 4 patients had a normal resting electrocardiogram. In patients with borderline accepted indications for surgery, calculation of the subendocardial flow index may be an additional useful variable in the timing of surgery.

Effect on training on myocardial oxygen supply/demand balance.

In five well-trained and five sedentary control subjects potential subendocardial blood supply was estimated from the diastolic pressure time index (DPTI) and myocardial oxygen demands from the tension time index (TII) during a progressive near-maximal treadmill test. DPTI/TTi was used to assess the effects of training on myocardial oxygen supply/demand balance. DPTI/TTI was significantly higher in trained subjects at rest and comparable workloads. At 6.4 km/hr, 18% grade (maximum for the controls), TTI was significantly lower (4300 +/- 76 vs 4495 +/- 99 mm Hg-sec/min) and DPTI significantly higher (2534 +/- 86 vs 2295 +/- 91 mm Hg-sec/min) in the trained subjects; DPTI/TTI was significantly higher (0.59 +/- .02 vs 0.50 vs .03). At near-maximal heart rates both groups achieved the same supply/demand balance (0.50); however, the trained subjects were working at higher workloads. We conclude that endurance conditioning increases work capacity, reduces myocardial O2 demands, increases potential O2 supply and improves the supply/demand balance at any given submaximal workload which reduces the risk of ischemia.

Coronary Circulatory Effects of Increased Intrathoracic Pressure in Intact Dogs

The effect of increased intrathoracic pressure on coronary hemodynamics and coronary venous oxygen tension was evaluated in surgically instrumented dogs. Following abrupt increase in intrathoracic pressure, as systolic pressure decrease, the tension time index (TTI) fell 83 percent (P less than 0.001) compared to control. The diastolic pressure time index (DPTI) decline proportionately less, effecting an increase in the ratio of DPTI/TTI from 1.19 +/- 0.08 to 1.78 +/- 0.16 (P LESS THAN 0.05). The mean circumflex coronary blood flow declined only minimally toward the end of the test (5.1 +/- 9.0 ml/min; P less than 0.05), and stroke systolic circumflex coronary blood flow increased 116 percent (P less than 0.01) as late diastolic coronary resistance decreased 31 percent (P less than 0.01). The mean coronary venous oxygen pressure increased transiently above control values from 21 +/- 1 to 24 +/- 2 mm Hg (P less than 0.05). These data suggest that in anesthetized dogs, brief periods of high intrathoracic pressure abruptly reduce determinants of myocardial demand for oxygen, while myocardial perfusion decreases to a lesser degree.

Intraoperative Application of Intraaortic Balloon Counterpulsation Determined by Clinical Monitoring of the Endocardial Viability Ratio

Persistent unrecognized subendocardial ischemia with development of subendocardial necrosis is a major cause of patient death following cardiopulmonary bypass. The lesion is caused by a discrepancy between the oxygen needs of subendocardial muscle and the available blood supply. If sole reliance is placed upon monitoring conventional vital signs, the more subtle factors contributing to decreased blood flow may go unrecognized. Reported studies have confirmed that the adequacy of subendocardial perfusion can be predicted by calculating the supply/demand ratio, defined as the ratio of the diastolic pressure-time index (DPTI) divided by the systolic pressure-time index (TTI). An analog computer was designed and built that measures the area under the systolic and diastolic component, calculates the DPTI/TTI ratio, and digitally displays the result as the endocardial viability ratio (EVR). The EVR was used to determine the adequacy of left ventricular subendocardial blood flow in 64 consecutive patients undergoing cardiac operations. Unidirectional intraaortic balloon counterpulsation (IABC) was utilized in 14 patients with 9 long-term survivors. The difference in mean EVR between survivors and nonsurvivors at the initiation of balloon support was statistically significant. Early application of unidirectional IABC when subendocardial ischemia persists following open cardiac procedures may prevent deterioration to subendocardial necrosis with subsequent morbidity or mortality.

Subendocardial blood flow in children with congenital aortic stenosis.

Subendocardial blood flow may be estimated from the ratio of flow to the subendocardium to myocardial oxygen consumption. The first may be estimated from the diastolic pressure time index (area between aortic and left ventricular (LV) pressure during diastole) and the latter by the tension time index (integral of LV pressure during systolic ejection). Subendocardial flow index (SEFI) averaged 1.27 (0.96-1.78) in 13 children with normal aortic valves. SEFI averaged 0.88 (0.43-1.65) in asymptomatic children with congenital aortic stenosis and was never greater than 0.9 in symptomatic children. Aortic valve area and systolic pressure difference did not correlate well with symptoms. SEFI and aortic valve area increased in 26 of 28 patients after surgery. However, 23 of 28 had varying degrees of aortic regurgitation following valvotomy. Since calculation of SEFI is not affected by aortic regurgitation, it would appear to be a more useful measure of surgical success than aortic valve area.

Myocardial metabolic studies in prolapsing mitral leaflet syndrome.

Patients with prolapsing mitral leaflet syndrome (PML) frequently have chest pain of undetermined etiology. Twenty-three patients with PML underwent cardiac hemodynamic, angiographic, and metabolic studies. The latter were performed during control spontaneous heart rate and tachycardia by right atrial pacing. Myocardial supply-demand ratio (DPTI:SPTI) was estimated from the planimetric integration of the diastolic area (diastolic pressure time index = DPTI) and systolic area (systolic pressure time index = SPTI) of the central aortic pressure. Chest pain during pacing occurred in five patients. In two patients, it was associated with ST depression typical of ischemia on the electrocardiogram. Myocardial lactate abnormalities (lactate production or less than 10% extraction) occurred in seven patients during pacing tachycardia and was present in two patients during control state. DPTI:SPTI ratio during control state was 1.22 (+/- 0.07 SE) and decreased to 0.85 (+/- 0.05 SE) during pacing tachycardia. It is concluded that the myocardial lactate abnormalities in PML, which were present in approximately 30% of the patients in the present series, are most likely due to myocardial hypoxia. Whether or not the hypoxia is secondary to "small vessel disease" is not elucidated by this study.

Ischemia in aortic stenosis: Hemodynamic prediction

The records of 12 patients with aortic stenosis previously studied by Fallen et al. 1 in 1967 before and after infusion of isoproterenol were reviewed to assess the value of hemodynamic indexes in predicting myocardial ischemia—defined as less than 5 percent transmyocardial lactate extraction or lactate production. Potential subendocardial blood supply was estimated from a diastolic pressure-time index (DPTI), calculated from aortic and left ventricular pressure, and oxygen demand, estimated from the tension-time index (TTI). The ratio DPTI TTI was used to estimate the supply/demand relation. Of eight patients with aortic stenosis but without associated coronary artery disease, four (Group A) metabolized lactate normally after administration of isoproterenol, and four (Group B) had biochemical evidence of ischemia. Three of four patients (Group C) with aortic stenosis and associated coronary artery disease had abnormal glycolysis after administration of isoproterenol. Calculated aortic valve areas were comparable in all groups. In patients with aortic stenosis alone, abnormal lactate metabolism occurred whenever DPTI/TTI was less than 0.30 ( P < 0.01) (Group B). Two of three patients with aortic stenosis and associated coronary artery disease (Group C) showed abnormal lactate metabolism when DPTI/TTI was greater than 0.6; this ratio was below 0.3 in the third patient. These results suggest that the supply/demand relation calculated from these readily obtained indexes may be useful (1) in predicting in which patients with aortic stenosis ischemia will develop, (2) in distinguishing the role played by associated coronary artery disease, and (3) as an adjunct to calculation of valve area since the quantitation of associated aortic regurgitation is not necessary.

The adequacy of subendocardial oxygen delivery: the interaction of determinants of flow, arterial oxygen content and myocardial oxygen need.

The interactions of determinants of subendocardial oxygen delivery (flow and oxygen content) and oxygen demand were studied. In open chest dogs, oxygen requirements were increased with aortic stenosis and oxygen delivery reduced with normovolemic anemia. We estimated potential subendocardial flow from a Diastolic Pressure Time Index (DPTI) and oxygen demands from the Tension Time Index (TTI), and detected ischemia with endocardial (Endo) and epicardial (Epi) electrocardiograms (ECG). Subendocardial oxygen delivery per unit of TTI was significantly lowered and Endo ECGs showed ischemia (ST elevation) when Endo/Epi flow ratios (microsphere method) fell below 1.0 ( P &lt; 0.001). Ischemia occurred without anemia (Hgb &gt; 10 g %) in severe aortic stenosis; with mild anemia (Hgb 5-10 g %) and mild aortic stenosis; and with severe anemia (Hgb &lt; 5 g %) without aortic stenosis. Ischemic Endo ECGs occurred with mild supravalvar aortic stenosis and mild anemia despite a 63% (92 to 150 cc/100g/min) average increase in subendocardial flow while Epi ECGs remained normal. Altered flow distributions and abnormal ECGs were always predictable from the ratio: DPTI x O 2 content (Supply)/TTI (Demand). These determinants of Supply and Demand are readily obtained from measurements of hemoglobin, saturation, and blood pressure.

Effects of perhexiline on symptomatic and hemodynamic responses to exercise in patients with angina pectoris

The effects of perhexiline on symptomatic and hemodynamic responses to exercise stress were evaluated in 16 patients with coronary artery disease and angina pectoris. Exercise-induced angina was prevented (12 of 16) or delayed during perhexiline treatment and exercise heart rate decreased (117.4 ± 6.1 [standard error of the mean] to 105.3 ± 3.6 beats/min, P < 0.05). Ischemia-related indexes of left ventricular dysfunction were attenuated (stroke work index 70.9 ± 5.7 to 86.4 ± 5.3 g-m/beat per m 2 and filling pressure 26.4 ± 3.0 to 17.7 ± 2.5 mm Hg, P < 0.01) without evidence for depression of other indexes of ventricular function. Additionally, the exercise diastolic pressuretime index increased 36.5 ( P < 0.01) and the diastolic pressure-time/ tension-time ratio increased 38 percent ( P < 0.05) with perhexiline in the patients who were free of angina. During increased exercise stress six patients achieved higher tension-time indexes before being limited by fatigue or dyspnea. The observed beneficial effects appear to be partly a result of reduced myocardial oxygen needs and improved oxygen supply.

ESTIMATION OF SUBENDOCARDIAL ISCHEMIA IN VALVAR AORTIC STENOSIS IN CHILDREN

Eighty-four cardiac catheterizations were reviewed in infants and children with isolated valvar aortic stenosis to evaluate the presence of subendocardial ischemia. An index of myocardial oxygen supply/demand was calculated from the left ventricular(LV) and aortic (Ao) pressure pulses. Supply was estimated by multiplying the area between Ao and LV pressures during diastole, i.e. Diastolic Pressure Time Index(DPTI), by arterial oxygen content(C). Demand was estimated by the systolic pressure time index(SPTI) from the area under the LV tracing during systole. The oxygen supply/demand ratio was expressed as: DPTI X C/SPTI. A ratio<10 has been shown experimentally in animals to be associated with a reduction in the LV subendocardial/subepicardial flow ratio. With severe stenosis (AVA<7cm2/m2) an increasing number of patients develop supply/demand ratios<10. Patients with AVA<.7cm2/m2 but heart rates (HR)<100/min maintain adequate ratios>10, whereas patients with severe stenosis and HR>100/min all have ratios<10 consistent with subendocardial ischemia. It is concluded that HR is a critical factor in the production of a reduced myocardial oxygen supply/demand ratio in patients with severe valvar aortic stenosis. This ratio is easily calculated from data obtained at cardiac catheterization and appears to be useful in identifying possible subendocardial ischemia in patients with aortic stenosis.

Left ventricular subendocardial ischemia in severe valvar and supravalvar aortic stenosis. A common mechanism.

Severe valvar aortic stenosis (VAS) and supravalvar aortic stenosis (SVAS) each may cause left ventricular (LV) subendocardial ischemia and infarction, even with patent coronary arteries. LV ischemia in VAS has been related to reduced coronary perfusion relative to raised metabolic requirements, whereas this mechanism of ischemia has not been widely accepted in SVAS because coronary perfusion pressure is higher than normal. LV subendocardial coronary blood flow (CBF) occurs predominantly in diastole and a diastolic pressure-time index (DPTI) was used to estimate it. LV oxygen requirements were estimated from the systolic pressure-time index (SPTI). The ratio DPTI:SPTI (supply:demand) was evaluated as an estimate of the adequacy of subendocardial flow. SVAS was produced acutely in nine dogs and phasic left CBF and distribution of CBF to the LV myocardium were measured. Although mean CBF always rose with aortic constriction, flow in diastole fell from a control of 80% to 34% ( P &lt; 0.001) and LV myocardial flow distribution became inhomogeneous with the proportion of flow to subendocardial muscle decreasing 63% ( P &lt; 0.001). Departure from the normal homogeneous flow distribution to the LV was predictable from the ratio DPTI:SPTI; values below 0.7 were always associated with relative subendocardial underperfusion. DPTI:SPTI ratios in two patients, one with severe VAS (0.25) and one with SVAS (0.39) were well below values obtained in 18 control patients (1.03 ± 0.23), and were similar to the ratios in dogs with SVAS (0.27 ± 0.08). Both patients had ECG changes suggesting LV ischemia. The mechanism of subendocardial ischemia is thought to be the same in both types of stenosis and its presence is predictable from pressure measurements available at cardiac catheterization.

Ischemic response to sudden strenuous exercise in healthy men.

In ten healthy, asymptomatic men, intra-arterial pressure and electrocardiograms were recorded during various types of exercise. Potential subendocardial blood flow was estimated from a diastolic pressure time index (DPTI) and myocardial oxygen requirements estimated from the tension time index (TTI). The ratio DPTI/TTI provided an estimate of the supply/demand relationship With sudden vigorous exercise without warm-up, the DPTI/TTI was below 0.35 in three men who had ischemic electrocardiograms, below 0.44 in three men with minor ST abnormalities, and above 0.44 in four men with normal ST segments. With a prior warm-up exercise, sudden exercise caused no ischemic changes, but DPTI/TTI was below 0.44 in two subjects who had minor ST abnormalities. Maximum treadmill testing produced higher heart rates and TTI than did sudden exercise, but DPTI/TTI was above 0.44 in all cases and no ST abnormalities occurred. Abnormal electrocardiographic responses produced by sudden, vigorous exercise in normal men may represent subendocardial ischemia caused by a transient, unfavorable alteration in the subendocardial oxygen supply/demand relationship which is predictable from arterial pressure measurements.

Effects of isoprenaline on coronary blood flow: its distribution and myocardial performance.

Isoprenaline was intravenously infused into open chest anaesthetized dogs and myocardial contractile force, cardiac output, and coronary blood flow distribution were monitored. The inotropic response to isoprenaline could be sustained only when the normally homogeneous left ventricular flow distribution was maintained. Contractile force fell when subendocardial muscle became underperfused relative to subepicardial muscle and was improved when coronary perfusion pressure and relative subendocardial flow were increased. Changes in flow distribution could be predicted from the ratio of the diastolic pressure time index and the tension time index (DPTI:TTI).