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Biomedical subjects

R G McKay

Publications and source records attributed to R G McKay.

90 records · Page 5Linked to original sources

Assessment of left ventricular and aortic valve function after aortic balloon valvuloplasty in adult patients with critical aortic stenosis.

Preliminary reports have documented the utility of balloon aortic valvuloplasty as a palliative treatment for high-risk patients with critical aortic stenosis, but the effect of this procedure on cardiac performance has not been studied in detail. Accordingly, 32 patients (mean age 79 years) with long-standing, calcific aortic stenosis were treated at the time of cardiac catheterization with balloon dilatation of the aortic valve, and serial changes in left ventricular and valvular function were followed before and after valvuloplasty by radionuclide ventriculography, determination of systolic time intervals, and Doppler echocardiography. Prevalvuloplasty examination revealed heavily calcified aortic valves in all patients, a mean peak-to-peak aortic valve gradient of 77 +/- 27 mm Hg, a mean Fick cardiac output of 4.6 +/- 1.4 liters/min, and a mean calculated aortic valve area of 0.6 +/- 0.2 cm2. Subsequent balloon dilatation with 12 to 23 mm valvuloplasty balloons resulted in a fall in aortic valve gradient to 39 +/- 15 mm Hg, an increase in cardiac output to 5.2 +/- 1.8 liters/min, and an increase in calculated aortic valve area to 0.9 +/- 0.3 cm2. Individual hemodynamic responses varied considerably, with some patients showing major increases in valve area, while others demonstrated only small increases. In no case was balloon dilatation accompanied by evidence of embolic phenomena. Supravalvular aortography obtained in 13 patients demonstrated no or a mild (less than or equal to 1+) increase in aortic insufficiency. Serial radionuclide ventriculography in patients with a depressed left ventricular ejection fraction (i.e., that less than or equal to 55%) revealed a small increase in ejection fraction from 40 +/- 13% to 46 +/- 12% (p less than .03). In addition, for the study group as a whole there was a decrease in left ventricular end-diastolic volume index (113 +/- 38 to 101 +/- 37 ml/m2, p less than .003), a fall in stroke-volume ratio (1.49 +/- 0.44 to 1.35 +/- 0.33, p less than .04), and no immediate change in left ventricular peak filling rate (2.05 +/- 0.77 to 2.21 +/- 0.65 end-diastolic counts/sec, p = NS). Serial M mode echocardiography and phonocardiography showed an increase in aortic valve excursion (0.5 +/- 0.2 to 0.8 +/- 0.2 cm, p less than .001), a decrease in time to one-half carotid upstroke (80 +/- 30 to 60 +/- 10 msec, p less than .001), and a small decrease in left ventricular ejection time (0.44 +/- 0.03 to 0.42 +/- 0.02 sec, p less than .001).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Combined percutaneous aortic valvuloplasty and transluminal coronary angioplasty in adult patients with calcific aortic stenosis and coronary artery disease.

Of 120 consecutive balloon aortic valvuloplasty procedures for critical aortic stenosis, valvuloplasty was performed in combination with coronary angioplasty in nine patients (average age 76 years). All nine patients were symptomatic with angina and congestive heart failure before combined procedures. Aortic valvuloplasty was performed with 20 to 23 mm balloon catheter advanced retrogradely from the femoral artery and resulted in an improvement in peak aortic valve gradient (60 +/- 19 to 33 +/- 13 mm Hg; p less than or equal to .01) and calculated aortic valve area (0.7 +/- 0.1 to 1.1 +/- 0.3 cm2; p less than or equal to .01). Single-vessel coronary angioplasty was performed via the femoral approach, with 2.0 to 3.5 mm balloon catheters, and resulted in a mean reduction of a critical coronary stenosis in each patient from 91 +/- 4% to 29 +/- 8%. The site of coronary angioplasty was the left anterior descending artery in three patients, the circumflex artery in three patients, the right coronary artery in two patients, and a bypass graft to the right coronary artery in one patient. Combined procedures were performed with a mean arterial time of 108 min. Complications included groin hematomas (n = 2), transient left bundle branch block (n = 1), and transient atrial fibrillation (n = 1). No patient experienced prolonged chest pain, myocardial infarction, major increase in aortic insufficiency, or embolic phenomena. Eight of the nine patients treated with combined procedures noted significant improvement in symptoms of angina and congestive heart failure and were discharged.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Comparison of methods for determining absolute left ventricular volumes from radionuclide ventriculography.

Several radionuclide techniques have been used in routine clinical nuclear medicine practice as a means of quantitating left ventricular chamber volumes in man. Despite wide use and availability of the different techniques, however, there has not been a thorough comparison of radionuclide and contrast angiographic measurements performed in the same patients in close temporal proximity. Accordingly, in order to validate traditional methods of ventricular volume measurement, we have performed contrast ventriculography followed immediately (upon return of baseline hemodynamics) by gated radionuclide ventriculography in 34 patients undergoing diagnostic cardiac catheterization. Absolute left ventricular end-diastolic volumes were determined from single-plane, right anterior oblique, end-diastolic contrast silhouettes using a standard area-length method. Radionuclide ventriculographic volumes were determined by three methods: planimetry (32 patients), counts-based (19 patients), and thermodilution stroke volume/radionuclide ejection fraction (32 patients). With planimetry, an area-length method was used in which the modified left anterior oblique left ventricular image was assumed to be a prolate ellipsoid whose volume can be determined by measuring surface area and the ventricular long axis. With the counts-based technique, a blood sample was drawn at the midpoint of the radionuclide ventriculogram acquisition and counted with a gamma camera with appropriate attenuation factor correction. With the thermodilution stroke volume/radionuclide ejection fraction technique, the left ventricular stroke volume was determined by dividing thermodilution cardiac output by the heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗

Percutaneous mitral valvuloplasty in an adult patient with calcific rheumatic mitral stenosis.

A 75 year old man with long-standing rheumatic mitral stenosis who refused surgical intervention was treated with percutaneous balloon valvuloplasty. Prevalvuloplasty evaluation revealed a heavily calcified mitral valve, a mean transvalvular gradient of 18 mm Hg, a Fick cardiac index of 1.7 liters/min per m2, a mitral valve area of 0.6 cm2 and 1 + mitral regurgitation. After transeptal catheterization and balloon dilation of the interatrial septum with an 8 mm angioplasty balloon, a 25 mm valvuloplasty balloon was advanced over a guide wire across the interatrial septum and positioned across the mitral anulus. Subsequent balloon inflation at 3 atm pressure resulted in a reduction of the mean mitral valve gradient to 12 mm Hg, an increase in cardiac index to 2.5 liters/min per m2, an increase in mitral valve area in 1.4 cm2 and an increase in mitral regurgitation from 1 + to 2 +. Valvuloplasty was well tolerated without embolization of clot or valvular debris, and resulted in marked clinical improvement with decreased dyspnea and increased exercise tolerance. Repeat catheterization 2 months after valvuloplasty showed further resolution of pulmonary hypertension and no evidence of valvular restenosis or worsening mitral regurgitation, but detected a small atrial septal defect with a pulmonary to systemic blood flow ratio of 1.8. It is concluded that percutaneous valvuloplasty is possible in the adult patient with calcific rheumatic mitral stenosis, and may result in a significant improvement in valvular function without producing life-threatening complications.

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Assessment of left ventricular end-systolic pressure-volume relations with an impedance catheter and transient inferior vena cava occlusion: use of this system in the evaluation of the cardiotonic effects of dobutamine, milrinone, Posicor and epinephrine.

The end-systolic pressure-volume relation has been postulated as a load-independent measure of cardiac contractility, but has been difficult to measure because of technical problems associated with the serial measurement of intracardiac volume over a physiologic range of ventricular loading conditions. Utilizing a multielectrode impedance catheter to assess continuous, on-line left ventricular relative volume during transient inferior vena cava occlusion, a method is described for determining the end-systolic pressure-volume relation and for assessing changes in this relation secondary to inotropic modulation. In particular, using this method, the relative inotropic properties were determined of four drugs: dobutamine, milrinone, epinephrine and an experimental cardiotonic agent (Ro 13-6438, Posicor). Left ventricular micromanometer pressure and impedance catheter volume were measured continuously in 10 open chest, anesthetized dogs and 14 pigs. Arterial pressure was altered over a range of 20 to 60 mm Hg by brief inferior vena cava constriction. A linear end-systolic pressure-volume relation was observed in pressure-volume diagrams constructed from on-line pressure and impedance catheter recordings. Administration of dobutamine, milrinone and epinephrine resulted in a leftward shift and an increase in the slope of the end-systolic pressure-volume relation as compared with baseline; Posicor did not alter the slope over a range of doses, despite an increase in the cardiac output secondary to arterial vasodilation. Volume changes as measured by the impedance method closely paralleled simultaneous changes in the ultrasonic crystal-determined segment length, and the impedance end-systolic pressure-volume relation slope was reproducible with repeated load-altering maneuvers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Right atrial pressure-volume relationships in tricuspid regurgitation.

Pressure-volume relationships in the right atrium were examined before and after the creation of acute experimental tricuspid regurgitation in pigs. A 1.3 kHz multielectrode impedance catheter with a measuring current of 4 mA was used to determine instantaneous right atrial pressure and relative blood volume; right atrial dimension was assessed simultaneously with ultrasonic crystals attached to the atrial walls. Impedance volume waveforms and ultrasonic crystal dimensions closely paralleled each other at baseline and after the induction of tricuspid regurgitation. The normal right atrial pressure-volume plot exhibited a figure-of-eight configuration, with an "a-loop" and a "v-loop" corresponding to the a-wave and v-wave of the right atrial pressure tracing. With severe tricuspid regurgitation, atrial pump function was abolished, and the pressure-volume plot exhibited a single clockwise loop, consistent with complete ventricularization of the right atrium. Intermediate degrees of tricuspid regurgitation preserved the figure-of-eight loop, but the size of both the a-loop and the v-loop were increased, consistent with a Starling-type load imposed on the atrium by the regurgitant blood volume. Increased right ventricular afterload mediated by constriction of the pulmonary artery and infusion of methoxamine reversibly converted the right atrial pressure-volume loop from that of mild to that of severe tricuspid regurgitation. Alternatively, constriction of the inferior vena cava and infusion of nitroprusside changed the right atrial pressure-volume loop from that of a severe pattern of tricuspid regurgitation to a less severe type of pattern. Infusion of dobutamine increased the size of the a-loop relative to the v-loop both at baseline and after induction of tricuspid regurgitation. We conclude that tricuspid regurgitation induces changes in right atrial mechanics that can be detected and quantified with an impedance catheter.

Animals↗

Balloon dilatation of calcific aortic stenosis in elderly patients: postmortem, intraoperative, and percutaneous valvuloplasty studies.

To assess the safety and efficacy of percutaneous balloon valvuloplasty in calcific aortic stenosis, balloon dilatation of critically stenosed, calcified aortic valves was performed in five postmortem hearts, in five patients intraoperatively before aortic valve replacement, and in two elderly patients percutaneously at the time of diagnostic catheterization. The etiology of aortic stenosis in the 12 cases was rheumatic in two, congenital bicuspid calcific stenosis in one, and senile calcific degenerative stenosis in the remaining nine. Prevalvuloplasty examination in the 10 postmortem and intraoperative cases revealed rigid valve leaflets with commissural fusion in three valves and extensive nodular calcification in seven. Subsequent balloon dilatation with 15 to 18 mm valvuloplasty balloons resulted in decreased cusp rigidity and increased mobility of valve leaflets in all cases, without evidence of tearing of valve leaflets, disruption of the valvular ring, or liberation of calcific or valvular debris. In the three valve specimens with commissural fusion, balloon dilatation resulted in partial or complete separation of leaflets along fused commissures. In two cases with extensive nodular calcification, balloon dilatation resulted in a fracture of a calcified leaflet that was evident on both gross and radiologic examination. After postmortem and intraoperative studies, percutaneous catheter valvuloplasty was performed at the time of diagnostic catheterization in two elderly patients (93- and 85-year-old women) with long-standing calcific aortic stenosis. Balloon dilatation with 12 to 18 mm balloons resulted in significant decreases in aortic gradients and significant increases in cardiac index and aortic valve area in both patients. Percutaneous valvuloplasty in both patients resulted in a mild increase in aortic insufficiency and no evidence of embolic phenomena.

Aged↗

Assessment of the end-systolic pressure-volume relationship in human beings with the use of a time-varying elastance model.

The analysis of left ventricular end-systolic pressure-volume relationships in human beings has been hindered by the lack of a practical method of serial volume assessment and by an imprecise definition of end-systole. Modifications of the end-systolic relationship that have been used to circumvent these problems have included the use of single-point end-systolic pressure-volume ratios, the use of peak systolic pressure/minimum ventricular volume points for end-systolic points, and the use of end-ejection as a marker for end-systole. To assess the correlation between the parameters generated by these modifications with the slope (Emax) and volume intercept (VO) of the end-systolic line as defined by Sagawa's model of time-varying elastance, simultaneous measurement of left ventricular pressure and gated radionuclide volume was made in 26 patients under various loading conditions and pressure-volume diagrams were constructed for each loading condition from 32 simultaneous pressure-volume coordinates. Two pressure-volume diagrams were recorded in 14 patients and three pressure-volume diagrams were recorded in 12 patients. Emax and VO were determined in all patients from the slope and volume intercept of the isochronic pressure-volume line with the maximum time-varying elastance as described by Sagawa's model and were designated true Emax and true VO, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion.

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p less than .01), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p less than .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p less than .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p less than .05) and significant increases in angiographic cardiac index (p less than .01) and LVESV index (p less than .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akinetic-dyskinetic segments and volume-overload hypertrophy of noninfarcted segments.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

The use of an exchange guide wire in coronary angioplasty.

Of 84 consecutive patients referred for coronary angioplasty, an exchange length (260 cm) guide wire was used in 17 (20%) to allow serial passage of different sized dilatation catheters. Exchanges were performed for the following reasons: 1) inability to cross the stenotic segment with a full-sized dilatation catheter, with exchange for a smaller catheter to permit initial dilatation followed by a second exchange to reintroduce the full-sized balloon catheter; 2) premeditated initial use of a low-profile balloon catheter in severe stenosis, with subsequent exchange to a full-sized balloon catheter; 3) inability to achieve a satisfactory reduction of the transstenotic gradient or angiographic stenosis with the initial dilation catheter, requiring subsequent passage of a larger balloon catheter into the partially dilated segment. Eighteen of 19 attempted exchanges and 18 of 19 angioplasty procedures were completed successfully. The use of exchange guide wires permits multiple recrossings of a dilated segment, allows safe serial passage of different sized balloon catheters, and obviates the need for renegotiating difficult proximal coronary anatomy. The exchange guide wire techique can be applied safely and effectively to coronary angioplasty and provides an additional option in the successful completion of movable guide wire angioplasty procedures.

Adult↗

Simultaneous assessment of left ventricular systolic and diastolic dysfunction during pacing-induced ischemia.

Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

The pacing stress test: a reexamination of the relation between coronary artery disease and pacing-induced electrocardiographic changes.

Electrocardiographic (ECG) changes during graded pacing-induced tachycardia have been considered unreliable as a test for the presence of coronary artery disease (CAD) because of poor sensitivity and specificity. As a result, atrial pacing has not been widely used as an alternative to exercise testing. However, the limited value of the pacing stress test may be related to technical aspects, such as the duration of pacing and ECG monitoring. To study this problem, 22 patients undergoing coronary cineangiography underwent standard exercise stress testing and graded tachycardia induced by atrial pacing. A 12-lead ECG recorder was used for both tests. Pacing tachycardia was terminated when 85% of maximal predicted heart rate had been achieved or when significant ischemic chest pain accompanied by diagnostic ECG changes occurred. The ECG was considered positive if at least 1 mm of horizontal or downsloping ST-segment depression was present. Six patients with normal or minimally diseased coronary arteries were compared to 16 patients with significant CAD. Of the patients without significant CAD, 5 (83%) had a negative electrocardiogram during both exercise and pacing. Of 16 patients with CAD, the electrocardiogram was positive for ischemia in 10 patients (63%) during exercise, in 15 (94%) during atrial pacing and in 12 (80%) after pacing. When the presence or absence of ECG changes was compared between the exercise and the pacing tests, there was a concordance of 90% (Fisher p less than 0.0015). Two patients without significant CAD (33%) had chest pain during both exercise and pacing. Among patients with CAD, 7 (44%) had chest pain during exercise and 8 (50%) had chest pain during atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

Left ventricular pressure-volume diagrams and end-systolic pressure-volume relations in human beings.

Assessment of left ventricular pressure-volume relations serially in response to altered loading conditions and heart rate has been difficult to achieve with contrast ventriculography. Accordingly, to study changing pressure-volume relations during altered loading and heart rate, left ventricular pressure and radionuclide absolute volume curves (obtained using a counts-based method with attenuation factor corrections) were recorded in 20 patients. Ventricular pressure and radionuclide volume curves were digitized and synchronized to end-diastole, and pressure-volume plots were subsequently constructed from 32 pressure-volume coordinates throughout the cardiac cycle. In all patients, the correlation between radionuclide absolute volumes and angiographic ventricular volumes was r = 0.92. In 10 patients in whom both radionuclide and angiographic pressure-volume diagrams were constructed, the agreement between the two methods was excellent. With this method, end-systolic pressure-volume relations were examined during altered left ventricular loading conditions, pacing-induced incremental increases in heart rate and pacing-induced ischemia. Using pharmacologically induced changes in left ventricular loading conditions, the slope and volume intercept of the end-systolic pressure-volume line could be calculated as a means of assessing basal contractility. During pacing-induced tachycardia, the slope and volume intercept of the end-systolic pressure-volume line could be calculated to quantify the Treppe effect and assess negative inotropic changes secondary to ischemia. This study supports the validity of using serial recordings of left ventricular pressure and radionuclide volumes to assess left ventricular pressure-volume relations, and indicates that this approach may be useful in the analysis of end-systolic pressure-volume relations in patients.

Cardiac Pacing, Artificial↗

The pacing stress test: thallium-201 myocardial imaging after atrial pacing. Diagnostic value in detecting coronary artery disease compared with exercise testing.

Many patients suspected of having coronary artery disease are unable to undergo adequate exercise testing. An alternate stress, pacing tachycardia, has been shown to produce electrocardiographic changes that are as sensitive and specific as those observed during exercise testing. To compare thallium-201 imaging after atrial pacing stress with thallium imaging after exercise stress, 22 patients undergoing cardiac catheterization were studied with both standard exercise thallium imaging and pacing thallium imaging. Positive ischemic electrocardiographic changes (greater than 1 mm ST segment depression) were noted in 11 of 16 patients with coronary artery disease during exercise, and in 15 of the 16 patients during atrial pacing. One of six patients with normal or trivial coronary artery disease had a positive electrocardiogram with each test. Exercise thallium imaging was positive in 13 of 16 patients with coronary artery disease compared with 15 of 16 patients during atrial pacing. Three of six patients without coronary artery disease had a positive scan with exercise testing, and two of these same patients developed a positive scan with atrial pacing. Of those patients with coronary artery disease and an abnormal scan, 85% showed redistribution with exercise testing compared with 87% during atrial pacing. Segment by segment comparison of thallium imaging after either atrial pacing or exercise showed that there was a good correlation of the location and severity of the thallium defects (r = 0.83, p = 0.0001, Spearman rank correlation). It is concluded that the location and presence of both fixed and transient thallium defects after atrial pacing are closely correlated with the findings after exercise testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The pacing stress test reexamined: correlation of pacing-induced hemodynamic changes with the amount of myocardium at risk.

To assess the relation between extent of ischemia and the magnitude of hemodynamic changes, 25 patients (5 with normal coronary arteries and 20 with significant coronary obstructive disease) were studied with rapid atrial pacing and thallium scintigraphy at the time of cardiac catheterization. Hemodynamic variables were measured before, during and after maximal pacing. Thallium was injected intravenously during maximal pacing and scans in three standard views were obtained immediately in the catheterization laboratory, with delayed scans obtained 4 hours after the cessation of pacing. The three thallium scans were each subdivided into five segments, and a thallium score was obtained on the basis of the total number of segments that were hypoperfused. Each patient was assigned a total thallium score corresponding to thallium defects at maximal pacing, as well as a redistributed thallium score corresponding to the difference between thallium score at maximal pacing and that 4 hours later. With pacing, patients with normal coronary arteries demonstrated no significant change in baseline hemodynamic variables, whereas patients with coronary artery disease exhibited a decrease in cardiac index, an increase in systemic vascular resistance, a widening of arteriovenous oxygen difference, an increase in pulmonary capillary wedge pressure and mean pulmonary artery pressure during maximal pacing and an increase in left ventricular end-diastolic pressure immediately after pacing. There was a significant correlation (Spearman rank r = 0.64, p less than 0.01) between redistributed thallium score and an increase in left ventricular end-diastolic pressure in the postpacing period. Moreover, there was an even higher correlation (Spearman rank r = 0.90, p less than 0.001) between total thallium score and the postpacing increase in end-diastolic pressure. It is concluded that in patients with coronary artery disease the magnitude of pacing-induced hemodynamic changes reflects both the amount of myocardial tissue at ischemic jeopardy and the total mass of hypoperfused myocardium during maximal pacing stress.

Adult↗

Instantaneous measurement of left and right ventricular stroke volume and pressure-volume relationships with an impedance catheter.

The feasibility of using continuous on-line recording of intraventricular electrical impedance to measure ventricular stroke volume was assessed in 12 patients at cardiac catheterization with a multielectrode impedance catheter and a 1.3 kHz measuring current of 4 microA. Stroke volumes determined by electrical impedance were compared with stroke volumes determined by the thermodilution technique in 10 patients and correlated with an r value of .95. Directional changes in impedance recordings throughout the cardiac cycle were also compared with volume curves obtained from six patients by radionuclide ventriculography, and in all instances the agreement between the two volume recordings was excellent. For all patients, on-line measurements of impedance showed a beat-by-beat decrease in stroke volume with the Valsalva maneuver and the administration of amyl nitrite, as well as an immediate increase in stroke volume in the contraction following an extra-systolic beat. Similar directional changes in stroke volume were recorded in both left and right ventricles. Left ventricular pressure-volume relationships were assessed with simultaneous left ventricular pressure recordings and volume signals recorded from the impedance catheter to determine if impedance measurements of volume can be used clinically. Pressure-volume diagrams were subsequently plotted, and for all patients these diagrams showed characteristic isovolumetric contraction and relaxation phases as well as typical ejection and filling periods. Moreover, beat-by-beat sequential pressure-volume diagrams constructed for patients during the administration of amyl nitrite revealed a linear end-systolic pressure-volume relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone.

To elucidate the mechanisms by which the new bipyridine inotropic agent milrinone improves cardiac function, we examined multiple indexes of left ventricular diastolic function before and after administration of milrinone to patients with advanced (NYHA class III or IV) congestive heart failure. In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone. In nine patients radionuclide ventriculographic studies were performed during left heart catheterization, allowing calculation of left ventricular peak filling rate, volumes, and the diastolic pressure-volume relationship before and after milrinone. After intravenous administration of milrinone, peak negative dP/dt increased (+ 18%; p less than .01) and T decreased (-30%; p less than .01), while heart rate increased by only 8% (87 +/- 12 to 94 +/- 15 beats/min; p less than .01), left ventricular systolic pressure did not change, and mean aortic pressure fell by 11% (p less than .01). Left ventricular peak filling rate increased (1.2 +/- 0.6 to 1.7 +/- 0.7 end-diastolic volumes/sec; p less than or equal to .02) despite a decrease in left ventricular filling pressure (mean pulmonary wedge pressure 27 +/- 7 to 18 +/- 9 mm Hg; p less than .01). There was a fall in left ventricular end-diastolic pressure (28.6 +/- 6 to 19 +/- 7 mm Hg; p less than or equal to .01), with no significant change in left ventricular end-diastolic volume. This was associated with a downward shift in the left ventricular diastolic pressure-volume relationship in most cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗