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It is now recognized that a sizable portion of patients who exhibit symptoms of congestive heart failure have relatively well-preserved systolic function, but have significantly elevated LV filling pressures. This syndrome, termed "diastolic heart failure," is associated with various conditions such as aging, anatomic abnormalities, hypertension, ischemic disease, tachycardia, and atrial fibrillation. Advances in the proper medical and surgical management of these patients will depend on the continued delineation of the basic physiologic mechanisms that account for normal and pathologic cardiac diastolic function. This goal can only be achieved by the integration of information acquired from basic science investigations conducted in vitro and in vivo, mathematic modeling simulation studies, and prospective, community-based investigations that characterize the incidence, prevalence, and natural history of the disease. In addition, randomized clinical trials will be needed to determine the optimal treatment strategies for this group of patients--strategy choices undoubtably complicated by a disease whose treatment is influenced to a large extent by its origin. The future therapies evaluated in these randomized clinical trials will most likely range from medical therapies that target either the heart directly or the peripheral vascular system, to surgical interventions such as direct myocardial revascularization, to gene therapy. Finally, it is worth mentioning one more unresolved issue that is of general practical concern not only to the physiologist studying diastolic function, but also to the clinician: whether or not it is even feasible to develop a single, sensitive, specific, clinically relevant index of diastolic function that is free from the contaminating influences of rate, contractility, and load. As observed by Glantz 20 years ago, developing indexes with the hope that one might fully delineate the left ventricle's diastolic properties, rather than concentrating on discovering the physiologic significance of such indexes, is probably counterproductive. More recently, in a related article, Slinker implied that an operational definition of any aspect of cardiac function must allow for the measurement of that function over an adequate range of essential variables. Therefore, as previously mentioned, the physiologist studying cardiac function has the daunting task of trying to understand, in a precise way, how the processes and mechanisms of the various phases of the cardiac cycle couple together to produce either a normal or abnormal functioning heart. It seems clear that because of the complex weave of factors that control overall cardiac diastolic function, the derivation of any single index that adequately describes LV diastolic function in vivo may not be possible.

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BACKGROUND: Although saphenous vein graft (SVG) markers have been available for many years, they have not been widely used in coronary artery bypass graft (CABG) surgery. This is likely due to the paucity of data regarding the utility of these markers in postsurgery cardiac catheterization. METHODS: We performed a prospective study of all post-CABG patients undergoing cardiac catheterization at Barnes-Jewish Hospital over a 6-month period to test our hypothesis that SVG markers would have a beneficial effect on these procedures. Differences in total procedure (arterial) time, time to image only the SVGs, fluoroscopy time, amount of contrast used, number of aortotomies, and number of views required were compared in patients with and without markers. RESULTS: Post-CABG patients undergoing catheterization who had markers (n = 76) required significantly less total procedure time (p = 0.007), fluoroscopy time (p = 0.02), and contrast use (p = 0.008). Even after adjusting for the numbers of SVG ostia and numbers of cine views, patients with markers still required less catheterization and fluoroscopy time (p < 0.01, p < 0.02) and time to image only the SVGs (p < 0.05) than those without markers (n = 106). CONCLUSIONS: SVG markers improve the efficiency of post-CABG catheterizations; they decrease the exposure of patients and cardiologists to ionizing radiation, and they decrease the exposure of patients to potentially toxic contrast agents. SVG markers are beneficial to the vast majority of post-CABG patients.

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Sepsis is a major cause of death in intensive care units. Clinically, sepsis induces a number of physiologic and metabolic abnormalities, including decreased myocardial contractility and decreased plasma ionized calcium. There is debate about the proper therapy of hypocalcemia in sepsis because calcium administration may worsen cell function by causing intracellular Ca2+ overload. We investigated the effect of Ca2+ administration on myocardial systolic and diastolic function in an extensively utilized rat model of sepsis, i.e., the cecal ligation and puncture model (CLP). Approximately 24 h after CLP or sham surgery, rats were anesthetized and myocardial function assessed in vivo by a left ventricular Millar catheter and simultaneous two-dimensional guided M-mode echocardiography. Septic rats had a 28% decrease in peak left ventricular developed pressure, a 30% decrease in +dP/ dt, and a 23% decrease in -dP/dt (p < 0.05). Plasma ionized Ca2+ was decreased in septic compared with that in sham rats: 4.9 +/- 0.9 and 5.6 +/- 0.01 mg/dl, respectively (p < 0.05). CaCl2 improved both systolic and diastolic function and there was no evidence of adverse effects of Ca2+ even at supraphysiologic levels. Surprisingly, correction of decreased afterload in septic rats, using the pure alpha-agonist phenylephrine, caused normalization of all indices of cardiac contractility, indicating that the presumed decrease in cardiac function was due entirely to an effect of the decreased afterload to "unload" the left ventricle. We conclude that Ca2+ administration is not detrimental to cardiac function in the rat CLP model. Although the rat CLP model is widely utilized and reproduces many of the clinical hallmarks of sepsis, it does not cause intrinsic myocardial depression and, therefore, it may not be an appropriate model to investigate the clinical cardiac dysfunction that occurs in patients with sepsis.

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OBJECTIVE: Our objective was to study the ability of three-dimensional MR angiography with retrospective respiratory gating to reveal stenoses in proximal coronary arteries on source and projection images. CONCLUSION: Proximal coronary artery stenoses can be identified using three-dimensional MR angiography with retrospective respiratory gating, both with projection images and on source images alone. Reasons for missed lesions included collateral vessels and retrograde flow distal to complete occlusion and volume averaging of vessels with adjacent structures. Causes of false-positive interpretations included small foci of decreased signal intensity distal to complete occlusion, partial volume effects on individual partitions, and regions of distal vessels leaving the imaging plane.

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BACKGROUND: Contractile reserve, improvement in contractile function during inotropic stimulation, is a proposed marker of viable myocardium. This study was designed to address, in patients with left ventricular dysfunction due to chronic coronary artery disease, whether contractile reserve depends on myocardial blood flow. METHODS AND RESULTS: We studied 19 patients, at rest and during dobutamine, with 2D echocardiography for regional mechanical function and PET for regional myocardial blood flow ([(15)O]water) and oxygen consumption ([11C]acetate). Of 166 myocardial segments, 21 had normal systolic function, 56 were dysfunctional but contractile reserve-positive, and 89 were dysfunctional and contractile reserve-negative. Myocardial blood flow at rest was lower in contractile reserve-negative (0.41+/-0.18 mL x g(-1) x min(-1)) than in contractile reserve-positive (0.50+/-0.22 mL x g(-1) x min(-1)) and normal segments (0.55+/-0.20 mL x g(-1) x min(-1), P<.009). After dobutamine infusion, blood flow increased less in contractile reserve-negative (0.63+/-0.38 mL x g(-1) x min(-1)) than in contractile reserve-positive (1.28+/-0.65 mL x g(-1) x min(-1)) and normal segments (1.93+/-0.83 mL x g(-1) x min(-1), P<.0001). Likewise, myocardial oxygen consumption was lower at rest in contractile reserve-negative (clearance rate of [11C]acetate, 0.043+/-0.012 min(-1)) than in contractile reserve-positive (0.048+/-0.01 min(-1)) and normal segments (0.058+/-0.008 min(-1), P<.02). Myocardial oxygen consumption with dobutamine increased less in contractile reserve-negative (0.060+/-0.013 min(-1)) than in contractile reserve-positive (0.077+/-0.016 min(-1)) and normal segments (0.092+/-0.024 min(-1), P<.0001). Of segments defined as viable by PET, 54% were contractile reserve-negative and exhibited lower blood flow with dobutamine (0.72+/-0.36 mL x g(-1) x min(-1)) than with viable, contractile reserve-positive segments (1.29+/-0.70 mL x g(-1) x min(-1), P<.0001). CONCLUSIONS: Contractile reserve depends, in part, on the level of myocardial blood flow at rest and during inotropic stimulation.

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OBJECTIVE: The relationship between the left ventricular (LV) relaxation time constant and early diastolic filling is not fully defined. This study provides additional evidence that LV isovolumic pressure fall in the normal intact heart in response to certain interventions is not adequately described by a model of monoexponential decay and that its relationship to filling is complex. METHODS AND RESULTS: To gain further insight into the relationship between LV relaxation and early rapid filling we measured LV isovolumic relaxation rate, peak early filling velocity (E), LV volumes, and transmitral pressures at baseline and in the first postextrasystolic beat after a short-coupled extrasystole in 9 anesthetized dogs. Postextrasystolic isovolumic relaxation rate was slowed as measured by 3 commonly used time constants, while E was increased 32%. LV contractility and peak pressure were also increased, while LV end-systolic volume was decreased. LV minimum pressure was deceased, while the early diastolic transmitral pressure gradient was increased. Although all relaxation time constants measured over the entire isovolumic relaxation phase indicated slowed relaxation, direct measurement of isovolumic relaxation time indicated no change in relaxation rate. Calculation of the time constants and direct measurement of isovolumic relaxation time during early isovolumic pressure decay indicated slowed postextrasystolic pressure decay rate compared with baseline, while calculation of time constants and direct measurement of isovolumic relaxation time during late isovolumic relaxation indicated augmented postextrasystolic pressure decay rate versus baseline. CONCLUSIONS: This non-exponential behavior of LV isovolumic pressure decay in postextrasystolic beats after short-coupled extrasystoles provides further evidence that the relationship that exists between ventricular relaxation and early filling is not simple. The results are interpreted in terms of current theoretical formulations that attribute control of myocardial relaxation to the interaction between inactivation-dependent and load-dependent mechanisms.

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BACKGROUND: Many reference levels have been proposed for the measurement of intracardiac pressures, but none have met with universal acceptance. In the first part of our study, we evaluated 10 cardiologists' understanding of how hydrostatic pressure influences intracardiac pressures as measured with fluid-filled catheters. In the second part, we proposed and validated a new zero level (H): the uppermost blood level in the left ventricular (LV) chamber relative to the anterior chest wall for a patient in the supine position. A comparison was made of LV minimum diastolic pressure measured by reference to H versus measurements made with the zero level at midchest. METHODS AND RESULTS: Using two-dimensional echocardiography, we determined H in the LVs of seven normal patients (five male, two female; age, 49 +/- 9 years) undergoing routine cardiac catheterization. H was determined from a left parasternal short-axis view and calculated as the average distance between end diastole and end systole of the endocardium of the uppermost segment of the LV anterior wall below the fourth or fifth intercostal space of the left sternal border on the anterior surface of the chest wall, with the patient in the supine position. A micromanometer/fluid-filled lumen catheter was then positioned in the LV, and we compared the micromanometer LV minimum pressure (LVPmin) obtained when the reference fluid-filled transducer was aligned at midchest with the LVPmin obtained when the reference fluid-filled transducer was aligned at H. LVPmin referenced to a midchest fluid-filled external transducer was measured as 5.1 +/- 1.6 mm Hg (range, 2.4 to 7.2 mm Hg) versus -0.6 +/- 0.6 mm Hg (range, -1.6 to 0.4 mm Hg) when referenced to H (P < .001). A significant linear relation was found to exist between patient anterior-posterior chest diameter and the magnitude of hydrostatic pressure influences related to pressure referenced at midchest (r = .88; P < .01). CONCLUSIONS: External fluid-filled transducers should be used with the goal of removing hydrostatic pressure and other influences so that the presence of subatmospheric pressure during diastole in any of the cardiac chambers is accurately measured. To achieve this goal, intracardiac pressure should be referenced to an external fluid-filled transducer aligned with the uppermost blood level in the chamber in which pressure is to be measured. The current practice of referencing the zero level of LV diastolic pressure to an external fluid-filled transducer positioned at the midchest level results in systematic overestimation due to hydrostatic effects and produces physiologically significant error in the measurement of diastolic intracardiac pressure.

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The incidence of nephrotoxicity occurring with the nonionic contrast agent, iohexol, and the ionic contrast agent, meglumine/sodium diatrizoate, was compared in 1196 patients undergoing cardiac angiography in a prospective, randomized, double-blind multicenter trial. Patients were stratified into four groups: renal insufficiency (RI), diabetes mellitus (DM) both absent (N = 364); RI absent, DM present (N = 318); RI present, DM absent (N = 298); and RI and DM both present (N = 216). Serum creatinine levels were measured at -18 to 24, 0, and 24, 48, and 72 hours following contrast administration. Prophylactic hydration was administered pre- and post-angiography. Acute nephrotoxicity (increase in serum creatinine of > or = 1 mg/dl 48 to 72 hours post-contrast) was observed in 42 (7%) patients receiving diatrizoate compared to 19 (3%) patients receiving iohexol, P < 0.002. Differences in nephrotoxicity between the two contrast groups were confined to patients with RI alone or combined with DM. In a multivariate analysis, baseline serum creatinine, male gender, DM, volume of contrast agent, and RI were independently related to the risk of nephrotoxicity. Patients with RI receiving diatrizoate were 3.3 times as likely to develop acute nephrotoxicity compared to those receiving iohexol. Clinically severe adverse renal events were uncommon (N = 15) and did not differ in incidence between contrast groups (iohexol N = 6; diatrizoate N = 9). In conclusion, in patients undergoing cardiac angiography, only those with pre-existing RI alone or combined with DM are at higher risk for acute contrast nephrotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

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BACKGROUND: Left atrial pressure (LAP) is often believed to play a dominant role in the determination of left ventricular (LV) early diastolic filling. In a previous study we found no significant relation between LAP and LV early filling velocity (E) but found instead a relation between E and two determinants of LV myocardial shortening (contractility and afterload). To determine if such disparate results may be related to the data ranges of the independent variables in a given population of animals, we took advantage of the differential hemodynamic effects of two modes of volume expansion: saline and whole blood. METHODS AND RESULTS: Eighteen closed-chest anesthetized dogs were instrumented with micromanometers for measurement of LV, left atrial, and aortic pressures. LV volumes were obtained with use of contrast ventriculography, pressures by micromanometry, and transmitral flow-velocity by Doppler echocardiography. After obtaining baseline measurements, group 1 (n = 9) received rapid infusion of 500 to 650 mL of saline over 10 minutes, and group 2 (n = 9) received the same volume infusion of whole blood. In terms of two known determinants of E, infusion of saline resulted in a significant increase in LAP at the moment of mitral valve opening (X1) (1.5 +/- 0.9 to 5.7 +/- 1.4 mm Hg; P < .05) and a moderate decrease in the pressure decay rate during isovolumic relaxation (tau 1/2) (22.9 +/- 2.4 to 26.3 +/- 3.5 milliseconds; P < .05). When these two factors were entered together into a multiple regression analysis with E as the dependent variable, the overall correlation was found to be significant (R = .722; P < .008), with both independent variables contributing significantly to the relation. When factors related to myocardial shortening (afterload and contractility) were added to this relation, they did not significantly improve the prediction of E. Like saline, whole blood infusion augmented X1 (1.6 +/- 2.4 to 8.8 +/- 3.2 mm Hg; P < .05) and tau 1/2 (21.5 +/- 2.6 to 32.0 +/- 6.3 milliseconds; P < .05) but also significantly increased LV afterload as measured by aortic diastolic pressure (91 +/- 10 to 110 +/- 12 mm Hg; P < .05). Multiple regression analysis of X1 and tau 1/2 with E again revealed a significant relation (R = .761; P < .002), with both independent variables contributing significantly to the relation. However, in this case, addition of contractility and afterload to the regression significantly improved the relation (R = .909; P < .001), with all four independent variables now contributing significantly to the prediction of E. CONCLUSIONS: Combined with our previous results, this study indicates the degree to which experimental methods can have an impact on the delineation of the determinants of a phenomenon as complex as LV early diastolic filling. Which independent variables emerge as primary determinants can be strongly influenced by the experimenter's choice of experimental design and manipulations. Specifically, experiments using volume infusion to delineate the responses of the cardiovascular system to variations in loading must allow for the hemodynamic changes that are inherent in the choice of infusate and infusion technique, especially when those interventions may significantly alter blood oxygen-carrying capacity and, in turn, differentially modify factors that affect the magnitude of the early diastolic transmitral pressure gradient.

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Contrast agents used for cardiac angiography are different in regard to ionicity, osmolality and physiologic effects. The nonionic contrast media have been shown to have less toxic effects and a better safety profile than do higher osmolar agents. To better assess this risk, clinically stable patients undergoing cardiac angiography were stratified according to the presence of diabetes mellitus, and level of serum creatinine, and then randomized to receive either iohexol (Omnipaque 350) or sodium meglumine diatrizoate (Renografin 76). All adverse events that occurred during and immediately after angiography were tabulated. A multivariate model was used to identify patients at increased risk for adverse outcome. The 1,390 patients were randomized to iohexol (n = 696) or diatrizoate (n = 694). Significant differences were found in the number of patients with contrast media-related adverse (iohexol vs diatrizoate: 10.2 vs 31.6%; p < 0.001) and cardiac adverse (7.2 vs 24.5%; p < 0.001) events. Severe reactions and the need for treatment were more frequent with diatrizoate than with iohexol, but there was no difference in the incidence of death. The presence of New York Heart Association classification 3 or 4 and serum creatinine > or = 1.5 mg/dl predicted a higher incidence of adverse events as a result of contrast media alone. Use of iohexol is associated with a lower incidence of all types of adverse events during cardiac angiography than is diatrizoate.

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We have previously shown that myocardial perfusion can be quantified by positron emission tomography (PET) with 15O-labeled water (H2(15)O), as experimentally validated with radiolabeled microspheres in animal hearts. The purpose of our study was to determine whether myocardial nutritive perfusion reserve assessed with PET in human subjects was parallel to flow velocity reserve assessed in conductance vessels measured with intracoronary Doppler probes. We studied nine patients with chest pain and angiographically normal coronary arteries with intracoronary Doppler flow velocity assessments before and after administration of 16 micrograms of intracoronary adenosine. We also assessed myocardial nutritive perfusion with PET and H2(15)O before and after intravenous administration of dipyridamole (0.56 mg/kg). Perfusion reserve (the ratio of absolute values of myocardial perfusion after dipyridamole administration to perfusion at rest) estimated with PET (3.5 +/- 0.9 s.d.) correlated closely with flow velocity reserve (the ratio of hyperemic intracoronary flow velocity to flow velocity at rest) (3.5 +/- 1.2, r = 0.80, p < 0.01). Absolute values of perfusion assessed tomographically averaged 1.22 +/- 0.19 ml/g/min in patients at rest and 4.16 +/- 0.93 after dipyridamole administration. Our data indicate that noninvasive assessment of myocardial perfusion with PET provides results that parallel intracoronary Doppler flow velocity measurements. Because PET delineates nutritive perfusion throughout the heart in absolute terms, its use may facilitate detection of impaired coronary arterial function and enhance delineation of the efficacy of potentially therapeutic interventions in patients with chest pain and angiographically normal coronary arteries.

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Femoral arterial pseudoaneurysms or arteriovenous fistulae may sometimes complicate percutaneous femoral artery catheterization procedures. Most surgeons recommend prompt operative repair because of the unfavorable natural history of pseudoaneurysms or arteriovenous fistulae secondary to violent or accidental arterial trauma. However, the natural history of catheterization-induced pseudoaneurysms and arteriovenous fistulae has not been well documented. Accordingly, we prospectively studied the natural history of 22 pseudoaneurysms, 8 arteriovenous fistulae, and 3 combined lesions, identified by duplex scan in 32 patients following trans-femoral cardiac, peripheral vascular, or vascular access arterial catheterization procedures. Angiographic procedures were performed with the use of 5-8F introducer sheaths. A femoral artery complication was significantly more likely to result from coronary balloon angioplasty (9/304; 3.0%) than from diagnostic cardiac catheterization (21/2476; 0.8%) (p less than 0.003; chi square). Fourteen patients (13 pseudoaneurysms, 1 combined pseudoaneurysm/fistulae) underwent surgical repair. Pain and/or enlarging hematoma resulted in repair within two days of the diagnosis in 8 patients. The need for chronic anticoagulation prompted elective repair in 2 patients. A pseudoaneurysm was repaired in one patient five days following catheterization when it became painful. In three stable patients, asymptomatic pseudoaneurysms were repaired electively during another surgical procedure. There were no operative deaths. One patients (7%) developed a wound infection postoperatively. Eighteen patients (19 arterial lesions: 9 pseudoaneurysms, 8 arteriovenous fistulae, 2 combined pseudoaneurysms/arteriovenous fistulae) with improving symptoms and stable physical signs were followed by serial clinical evaluation and duplex scans. Seventeen of 19 (89%) of these lesions resolved spontaneously within 5-90 days (mean 30.7 days).(ABSTRACT TRUNCATED AT 250 WORDS)

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BACKGROUND: Three important determinants of left ventricular (LV) peak early diastolic filling rate, which is related directly to the magnitude of the transmitral pressure difference, are the rate of LV isovolumic pressure fall (T1/2), left atrial (LA) pressure at mitral valve opening (X1), and end-systolic volume (ESV). METHODS AND RESULTS: To delineate the relative degrees to which these factors contribute to the magnitude of peak early diastolic filling rate, we measured LA and regional intra-LV pressures with micromanometers, LV volume with contrast angiography, and peak transmitral flow velocity (E) with transesophageal Doppler echocardiography in 16 anesthetized closed-chest dogs. E did not correlate significantly with either X1 (r = -0.255) or T1/2 (r = -0.281). Multivariate analysis, with E entered as the dependent variable and X1 and T1/2 as independent variables, also failed to reach significance (R = 0.310). E correlated significantly with ESV (r = -0.633, p less than 0.009). Using multivariate analysis, the major determinants of ESV were found to be LV contractility (+dP/dt), afterload (aortic diastolic pressure, AOdias), and preload (end-diastolic volume, EDV) (R = 0.848, p less than 0.001). E correlated significantly with two of the determinants of ESV (+dP/dt and AOdias) (R = 0.906, p less than 0.001); however, the addition of EDV did not significantly improve the multivariate relation (R = 0.911). To determine whether X1 or T1/2 would add significantly to the above multivariate relation, these factors were entered individually along with +dP/dt and AOdias as third independent variables. Neither the addition of X1 (R = 0.906) or T1/2 (R = 0.926) resulted in a significant improvement in the prediction of E. CONCLUSIONS: Our observations confirm the importance of factors related to ESV as important determinants of early diastolic filling. These relations suggest that the process of early diastolic function is intimately related to systolic function.

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This study was designed to determine in patients with unstable angina whether specific electrocardiographic abnormalities associated with ischemia, the presence of coronary lesions consistent with thrombosis on angiography or the presence of recurrent ischemia reflects increases in thrombin activity as manifested by increased plasma concentrations of fibrinopeptide A. The concentration of fibrinopeptide A in plasma was increased to 6.7 +/- 3.1 nM for the group as a whole (n = 29). Increases were greater in the 17 patients who exhibited reversible ST segment shifts (10.2 +/- 5.2 nM) than in the 12 patients exhibiting reversible T wave abnormalities alone (1.6 +/- 0.2 nM) (p less than 0.01). Nine of the 17 patients with reversible ST segment shifts who underwent coronary angiography had lesions with morphologic characteristics consistent with atherosclerotic plaque complicated by thrombosis compared with only 2 of 9 patients with T wave changes only (p less than 0.05). Plasma concentrations of fibrinopeptide A were markedly elevated in 7 of the 11 patients in whom complex lesions were noted on angiographic examination. Thus, the occurrence of reversible ST segment shifts identifies a group of patients with unstable angina in whom ongoing thrombosis is likely and who may be particularly likely to benefit from antithrombotic therapy.

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PURPOSE: Patients with chest pain but without angiographic evidence of significant atherosclerotic coronary artery disease (CAD) are often found to have other medical or psychiatric disorders, including mitral valve prolapse, panic disorder (PD), and major depressive disorder (MDD). The purpose of this study was to determine the degree of comorbidity between MDD/PD and mitral valve prolapse in a group of patients with non-CAD chest pain. PATIENTS AND METHODS: Patients referred for cardiac catheterization and coronary angiography for suspected CAD who were 70 years of age or younger and without other significant medical illnesses or cardiac complications were eligible for study. The first 100 patients who agreed to a psychiatric diagnostic interview were recruited. RESULTS: Forty-eight of the 100 patients were found to be without significant CAD. Forty-two percent of these patients, compared to 19% of the patients with significant CAD, were found to have either MDD, PD, or both. Eighty percent of the patients without CAD who had mitral valve prolapse also had either MDD or PD (p less than 0.006). CONCLUSIONS: The finding that mitral valve prolapse was significantly associated with MDD/PD has implications for the diagnosis and treatment of patients with non-CAD chest pain, and may explain why these patients complain of symptoms.

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Regional intraventricular pressure gradients exist in the left ventricle (LV) during both the early and late filling phases of diastole. These regional pressure gradients comprise a fundamental component of the mechanism of normal LV filling. To determine whether similar diastolic pressure gradients also occur in the right ventricle (RV), we measured right atrial (RA) and RV regional pressures with use of micromanometers in six anesthetized, closed-chest dogs. Tricuspid flow velocity was recorded with use of transesophageal Doppler echocardiography, and right ventriculograms were obtained with contrast angiography. As in the LV, the maximum RA-RV pressure gradient during early diastole was consistently greater if RV pressure was measured near the apex than in the inflow tract (1.6 +/- 0.5 versus 0.8 +/- 0.4 mm Hg). The area of reversed pressure was also found to be significantly greater in the apex than in the inflow tract (72 +/- 43 versus 8 +/- 6 mm Hg.msec). However, unlike the LV, the lowest minimum pressure was usually recorded in the RV outflow tract, resulting in a significantly increased RA-RV outflow tract pressure gradient compared with the RA-RV apex pressure gradient (2.5 +/- 0.8 versus 1.6 +/- 0.5 mm Hg). Analysis of right ventriculograms indicates marked narrowing of the RV outflow tract at end systole in all six animals, suggesting that an end-systolic deformation in this region is the likely mechanism for production of low early diastolic pressure in this region. During atrial contraction the RV regional pressure gradient pattern was similar to the LV pattern: the RV a-wave ascent occurred earlier in the inflow tract and later in the apex. A-wave ascent appeared to occur almost simultaneously in the apex and outflow tract. In the six animals, Doppler-derived peak tricuspid flow velocity during early diastole was 35 +/- 6 cm/sec. Early tricuspid flow acceleration (393 +/- 101 cm/sec2) was found to be significantly greater than deceleration of flow (182 +/- 59 cm/sec2). Comparison of tricuspid pressure-flow data with mitral pressure-flow data previously obtained in our laboratory indicates that the driving pressure gradient across the tricuspid valve is significantly less than across the mitral. This pressure difference corresponds to differences in acceleration and peak flow found across the two valves. Consideration of these physiological patterns of RV diastolic intraventricular pressure and their relation to filling has important implications with regard to the development of indexes that characterize diastolic pressure-flow relations and provides physiological insight relating to the location of ventricular restoring forces.

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A consistent pattern of intraventricular regional pressure gradients exists under physiological conditions during the rapid filling phase of diastole in the normal dog left ventricle. We hypothesized that this pressure gradient pattern is caused, in part, by early diastolic recoil of the left ventricular walls in conjunction with release of elastic potential energy stored during systole, generating suction and thus contributing to diastolic filling. If so, any condition that interferes with normal regional systolic function might be expected to modify the pattern of the normal early diastolic intraventricular pressure gradients. Accordingly, the present study was designed to determine whether acutely induced regional systolic left ventricular mechanical dysfunction is accompanied by changes in the pattern of the early diastolic intraventricular pressure gradients. Acute myocardial ischemia was induced by balloon occlusion of the left anterior descending coronary artery (LAD) in nine anesthetized closed-chest dogs. The maximum early diastolic intraventricular pressure gradient (MIVP) was measured between the mid-left ventricle and apex with a dual-sensor micromanometer (3-cm spacing between the sensors) before and 20 minutes after LAD occlusion. Ejection fraction (EF) and number of dyskinetic chords (DChords) were measured from left ventricular contrast ventriculograms. Twenty minutes after LAD occlusion, the nine dogs evidenced significant changes in EF (56 +/- 10% to 37 +/- 8%), DChords (0 +/- 0 to 17 +/- 16 chords), left ventricular minimum pressure (-1.7 +/- 0.5 to 0.0 +/- 1.5 mm Hg), left ventricular end-diastolic pressure (4.2 +/- 1.2 to 5.9 +/- 2.2 mm Hg), and heart rate (90 +/- 17 to 103 +/- 18 beats/min).(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of coronary angioplasty on myocardial flow reserve have been difficult to characterize noninvasively because conventional imaging techniques cannot quantitate blood flow in absolute terms. The effects of coronary angioplasty on myocardial perfusion and perfusion reserve were delineated with positron emission tomography and oxygen-15-labeled water (H2(15)O) in 13 patients before and after single vessel angioplasty. In 11 patients, angioplasty was successful (minimal cross-sectional area increased from 0.60 +/- 0.59 to 3.45 +/- 1.09 mm2, p less than 0.001). In these patients, regional H2(15)O radioactivity (the ratio of nutritional perfusion in regions distal to the stenosis compared with regions supplied by angiographically normal arteries) at rest before angioplasty was 55 +/- 22% of peak myocardial radioactivity and did not increase significantly afterward (70 +/- 16%, p = NS). However, after administration of intravenous dipyridamole, hyperemic perfusion in regions distal to a stenosis averaged only 39 +/- 18% of peak myocardial counts before angioplasty, but increased to 66 +/- 22% after angioplasty (p less than 0.02). Perfusion reserve in the two patients in whom angioplasty was angiographically unsuccessful showed no change. Quantitative estimates of perfusion in absolute rather than relative terms were obtained with positron emission tomographic data from seven of the patients with successful angioplasty. At rest, perfusion in regions distal to a stenosis was not different from the values in regions supplied by normal coronary arteries (1.54 +/- 0.54 compared with 1.46 +/- 0.38 ml/g per min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

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