Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coronary artery disease.

Previous studies suggested that cigarette smoking 1) inhibits an increase in coronary blood flow that should occur with increased myocardial oxygen demands, and 2) alters thromboxane and prostacyclin production, causing vasoconstriction and platelet aggregation. In 38 smokers (26 men and 12 women, aged 50 +/- 8 years [mean +/- standard deviation] ) with coronary artery disease, systemic and coronary hemodynamic and serologic variables were measured before and after smoking two cigarettes (in 8 to 10 minutes) (21 patients) or 8 to 10 minutes without smoking (17 patients; control group). No variable changed in the control group. Smoking increased (p less than 0.05) heart rate-systolic pressure product, cardiac output and maximal first derivative of left ventricular pressure (dP/dt) without significantly changing the coronary sinus concentrations of thromboxane B2 or 6-keto-prostaglandin F1 alpha (the stable metabolites of thromboxane A2 and prostacyclin, respectively). Smoking did not increase coronary flow in 6 of 11 patients with greater than 70% stenosis of the proximal left anterior descending or circumflex coronary artery, or both, whereas it caused an increase in coronary flow in all 10 patients without proximal stenoses (p = 0.006). To determine if smoking altered the response of coronary flow to increased myocardial oxygen demands, 10 smokers (5 men and 5 women, aged 48 +/- 9 years) underwent atrial pacing for 5 minutes followed 15 minutes later by atrial pacing for 5 minutes during smoking. In the five patients without proximal left coronary artery stenoses, coronary flow increased 26 +/- 29 ml/min with pacing and 45 +/- 21 ml/min with pacing/smoking (p = 0.018).(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of myocardial performance in ischaemic heart disease: from changes in left ventricular power output produced by graded-dose isoprenaline infusion.

Current clinical indices of myocardial contractility derive from concepts of muscle mechanics developed from isolated muscle experiments. Numerous simplifying assumptions are needed to apply these concepts to contractility studies in the whole heart. An alternative is to consider the heart as a pump which generates both pressure (P) and flow (Q) and to estimate its performance from the power output of its ventricles (P X Q). A method is described for measuring peak left ventricular power output in patients during routine cardiac catheterisation. The measurements have been made at rest and following inotropic challenge with gradient infusions of isoprenaline intravenously. Results from 13 patients with coronary artery disease and severe angina pectoris, who were clinically indistinguishable from one another, are reported. The patients could be grouped according to their left ventricular peak power responses to isoprenaline, although no difference could be demonstrated between them at rest. The patients who showed no increase in left ventricular power response to isoprenaline had a poor prognosis.

Survival in congestive heart failure: have we made a difference?

Congestive heart failure (CHF) affects approximately 400,000 new patients each year in the United States, resulting in death in more than 50% within five years, with traditional therapy including digitalis and diuretics. The aging of the population will only serve to aggravate this problem. Surgical treatment of CHF is a viable option in a minority of cases; a total of no more than 2,000 heart transplantation procedures were performed in the United States in 1988. Therefore, if survival is to improve in patients with CHF, effective alternative medical therapy may need to be added to or substituted for more traditional therapy. Vasodilator therapy with the angiotensin-converting enzyme inhibitors captopril and enalapril, or the combination of hydralazine and isosorbide dinitrate, improves survival in patients with severe heart failure when added to treatment with digitalis and diuretics. Nevertheless, the mortality rate remains extremely high once this stage of the disease process is reached. The prevention of left ventricular dilatation and remodeling, before the occurrence of overt heart failure, is the focus of much attention. Interventions that limit or interrupt the disease process at an even earlier stage will be necessary to make a major impact on survival.

Left ventricular dysfunction due to chronic right ventricular pressure overload. Resolution following percutaneous balloon valvuloplasty for pulmonic stenosis.

Left ventricular dysfunction due to chronic right ventricular pressure overload is well documented in experimental animals, but is controversial in humans. Whether left ventricular dysfunction resolves following the relief of chronic right ventricular pressure overload has not been studied. In this report, rapid improvement in both right and left ventricular function following successful percutaneous balloon valvuloplasty is described in a patient with severe isolated valvular pulmonic stenosis and biventricular dysfunction. It appears that: (1) geometric distortion played a major role in his reversible left ventricular dysfunction, and (2) severe biventricular dysfunction should not be a contraindication to valvuloplasty for valvular pulmonic stenosis.

Radionuclide techniques for valvular regurgitant index: comparison in patients with normal and depressed ventricular function.

We compared contrast angiography with three techniques of quantitating valvular regurgitation from radionuclide ventriculograms in 70 patients: 45 with documented regurgitation graded 1-4+, and 25 without regurgitation. The radionuclide "regurgitant index" (ratio of L to R ventricular stroke counts) was measured from fixed end-diastolic regions of interest (method A), from separate end-diastolic and end-systolic regions of interest (method B), and from a "stroke-volume image" (method C). Sensitivities for detecting 1+ or more regurgitation were: method A = 57.8%, method B = 37.8% and method C = 62.2%. Sensitivities for detecting 2+ or more regurgitation were: method A = 74.2%, method B = 54.8%, and method C = 77.4%. All methods are greater than 97% specific. Interobserver coefficients of variability were: method A = 9.1%, method B = 19.2%, and method C = 5.4%. The sensitivity of each method was improved when left-ventricular ejection fractions were greater than 0.35. No method consistently differentiated between 2+, 3+, and 4+ valvular regurgitation.

Analysis of factors affecting the variability of Fick versus indicator dilution measurements of cardiac output.

This study was performed to assess the relation between Fick and indicator dilution measurements of cardiac output (CO) in a large number of subjects and to evaluate this relation in patients with a low CO, a high CO, and left-sided cardiac regurgitation. In 808 patients (428 men, 380 women, mean age 50 +/- 11), CO was measured by Fick and either thermodilution (right atrium to pulmonary artery)(n = 252) or indocyanine green dye ("dye")(pulmonary artery to systemic artery)(n = 556) within 10 minutes of each other. There was excellent agreement between Fick and both thermodilution and dye. The difference between Fick and indicator dilution measurements was 9 +/- 9%; it was 10% or less in 67% and 20% or less in 91% of patients. The disparity between Fick and indicator dilution measurements was increased in patients with a low CO (less than 2 liters/min/m2)(n = 152) (difference 14 +/- 11%, p less than 0.001) and those with aortic or mitral regurgitation (n = 83) (difference 13 +/- 11%, p less than 0.001). In these groups, the disparity between Fick and thermodilution measurements was not exaggerated, but the disparity between Fick and dye measurements was greater. Thus, although there is excellent agreement between Fick and both thermodilution and dye measurements of CO, thermodilution is preferable to dye in patients with a low CO and those with aortic or mitral regurgitation.

Variability of right-sided cardiac oxygen saturations in adults with and without left-to-right intracardiac shunting.

In many catheterization laboratories and intensive care units, oxygen saturation of single blood specimens is measured from the superior vena cava (SVC), right atrium (RA) and pulmonary artery (PA) during right-sided catheterization, but variability of such single measurements in adults with and without intracardiac left-to-right shunting has not been assessed. Oxygen saturation of SVC, RA and PA single blood samples were measured in 1,031 adults (524 men, 507 women, aged 50 +/- 13 years [mean +/- standard deviation SD]). In the 980 patients without shunting, differences in saturation between SVC and RA, RA and PA and SVC and PA were 3.9 +/- 2.4%, 2.3 +/- 1.7%, and 4.0 +/- 2.5%, respectively, so that the normal limits of variability (mean +/- 2 standard deviations) for these saturation differences were 8.7%, 5.7% and 9.0%, respectively. Of the 51 patients with left-to-right shunting, these limits of variability of oxygen saturation correctly identified 46 (90%), and the 5 with shunting whose saturation differences were below these limits had small shunts (Qp/Qs ratios of 1.9 or less). Thus, assessment of oxygen saturation from single blood specimens obtained from the SVC, RA and PA offers excellent sensitivity (more than 90%), specificity (94 to 95%) and predictive accuracy (94% or more) in identifying patients with and without intracardiac left-to-right shunting. The sensitivity of these limits is especially high in patients with large shunts (Qp/Qs of 2 or more).

Importance of the "atrial kick" in determining the effective mitral valve orifice area in mitral stenosis.

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 +/- 0.9 vs 5.2 +/- 0.8 liters/min at 110 beats/min, 4.2 +/- 0.9 vs 5.1 +/- 0.9 liters/min at 140 beats/min; p less than 0.05) and LV end-diastolic volume (77 +/- 27 vs 93 +/- 29 ml at 110 beats/min, 54 +/- 17 vs 65 +/- 19 ml at 140 beats/min; p less than 0.05), an increase in left atrial pressure (28 +/- 3 vs 20 +/- 5 mm Hg at 110 beats/min, 30 +/- 4 vs 25 +/- 5 mm Hg at 140 beats/min; p less than 0.05), and a decrease in mitral valve area (1.2 +/- 0.4 vs 1.4 +/- 0.5 cm2 at 110 beats/min, 1.2 +/- 0.4 vs 1.4 +/- 0.4 cm2 at 140 beats/min; p less than 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.

Left ventricular volumes by single-plane cineangiography: in vivo validation of the Kennedy regression equation.

This study was performed to assess the accuracy and reliability of the regression equations of Kennedy et al and Wynne et al in the quantitation of single plane left ventricular (LV) volumes. In 15 patients with normal LV function and without intracardiac shunting or valvular insufficiency, gated equilibrium blood pool scintigraphy was performed simultaneously with the measurement of cardiac output (by thermodilution), after which left ventriculography was performed in the 30 degrees right anterior oblique (RAO) projection. From the scintigraphically determined LV ejection fraction (EF) and the thermodilution-measured stroke volume (SV), absolute LV volumes were calculated. The cineangiographic LV volumes obtained with the regression equation of Kennedy et al closely approximated those calculated by scintigraphy/thermodilution, whereas the volumes determined using the regression equation of Wynne et al were larger (p less than 0.05) than the calculated volumes. In 204 patients without intracardiac shunting or valvular insufficiency, SV was measured by the Fick or indicator dilution methods, after which single-plane left ventriculography was performed in the 30 degrees RAO projection. In the 83 patients without coronary artery disease with normal (n = 69) or depressed (n = 14) LVEF, cineangiographic SV (obtained using the regression equation of Kennedy et al) closely approximated forward SV. Similarly, this relation was excellent in the 142 patients whose LVEFs were greater than or equal to 0.50.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathophysiologic mechanisms of cardiac tamponade and pulsus alternans shown by echocardiography.

A pericardial effusion is easily recognized by echocardiography, but the diagnosis of cardiac tamponade by echocardiography is controversial. Recently, several reports have indicated that right ventricular (RV) or right atrial (RA) diastolic collapse represent highly specific and sensitive signs of a hemodynamically significant pericardial effusion. This report evaluates the pathophysiologic significance of these findings in 3 patients. One patient had classic clinical and hemodynamic features of tamponade without typical echocardiographic features; 1 had typical echocardiographic features of tamponade without the characteristic clinical or hemodynamic features; and 1 had all the findings characteristic of tamponade, including mechanical and electrical alternans. The first patient had increased right-sided cardiac pressures and RV hypertrophy, which prevented RV or RA collapse. The second patient had low right-sided intracardiac pressures, which allowed RV and RA diastolic compression to occur during early and mid-diastole. In the third patient, severe holodiastolic impairment of right-sided filling, and presumed decreased pulmonary venous and pericardial compliance, in the setting of tamponade produced a beat-to-beat alternation of RV and left ventricular filling with associated electrical and mechanical alternans. RV or RA collapse during diastole occurs when intrapericardial pressure equals or exceeds intracardiac pressure. Increases in wall stiffness of chamber pressures may prevent diastolic collapse in the setting of tamponade. Conversely, extremely low intracardiac pressures may allow diastolic collapse to occur in the absence of overt cardiac tamponade. The extent and timing of the RA or RV collapse, rather than its mere occurrence, are important in the diagnosis of cardiac tamponade by echocardiography.

Direct measurement of cardiac output by gated equilibrium blood pool scintigraphy: validation of scintigraphic volume measurements by a nongeometric technique.

A nongeometric technique for the determination of left ventricular volumes from the count data derived from gated equilibrium blood pool scans was previously described and validated by the demonstration of an excellent correlation between the derived data and angiographically determined left ventricular volumes. To provide a further prospective evaluation of this method and to validate its ability to determine stroke volume and cardiac output by a technique that is itself independent of geometric assumptions, simultaneous measurements of cardiac output by the thermodilution technique and gated scintigraphy were performed in 21 patients without valve regurgitation or intracardiac shunts. To substantiate the reliability of scintigraphic measurements at high levels of cardiac output, seven patients had multiple measurements of cardiac output at rest and during an infusion of isoproterenol. There was an excellent correlation between thermodilution and scintigraphic values for cardiac output (scan cardiac output = 0.99 thermodilution cardiac output - 0.005 liters/min; n = 31, standard error of the estimate [SEE] = 0.175 liters/min, r = 0.97) as well as between thermodilution and scintigraphic stroke volumes (scan stroke volume = 1.03 thermodilution stroke volume - 2.8 ml; n = 31, SEE = 2.5 ml, r = 0.95). In addition, the relation between scintigraphic and angiographic measurements of left ventricular volumes continued to be excellent: In 15 patients with technically adequate angiograms, scintigraphic left ventricular volume = 0.90 angiographic left ventricular volume + 7 ml (n = 30, SEE = 10 ml, r = 0.91). Thus, this study further validates the nongeometric method of measuring left ventricular volumes with gated scintigraphy and demonstrates its ability to measure left ventricular stroke volume and cardiac output reliably.

Hemodynamic effects of intravenous prostacyclin in stable angina pectoris.

Prostacyclin (PGI2) is a naturally occurring vasodilator and inhibitor of platelet aggregation that produces vasodilatation of the systemic, pulmonary and coronary vascular beds in animal models. Because the endogenous production of PGI2 is reduced in those with coronary arterial disease (CAD), it may have a therapeutic role in patients with ischemic heart disease. To assess its safety and efficacy in this clinical setting, 17 patients with stable angina and CAD received an incremental intravenous infusion of either PGI2 (n = 10) to a maximum dose of 10 ng/kg/min (average 9.8 +/- 0.8 [mean +/- standard deviation]), or diluent buffer solution (placebo) (n = 7). All patients who received PGI2 became flushed, but experienced no other adverse effects PGI2 caused an increase in heart rate (66 +/- 11 to 80 +/- 11 beats/min, p less than 0.001) and cardiac index (2.88 +/- 0.65 to 3.97 +/- 1.17 liters/min/m2, p less than 0.001) and a decrease in mean femoral arterial pressure (96 +/- 18 to 86 +/- 11 mm Hg, p less than 0.001), but no change in mean pulmonary arterial or capillary wedge pressure. Total systemic and pulmonary vascular resistance decreased significantly (p less than 0.001). In response to PGI2, mean coronary sinus blood flow did not change significantly (100 +/- 40 to 121 +/- 52 ml/min), but coronary vascular resistance decreased (1.07 +/- 0.40 to 0.83 +/- 0.36 U, p less than 0.001). No variable was altered by placebo infusion. PGI2 caused a marked increase in 6-keto PGF1 alpha (the stable metabolite of PGI2) concentrations in both arterial (42 +/- 29 to 567 +/- 216 pg/ml, p less than 0.001) and venous (46 +/- 31 to 604 +/- 229 pg/ml, p less than 0.001) blood but no demonstrable change in plasma renin activity. Thus, intravenous PGI2 to a dosage of 10 ng/kg/min is a safe and effective systemic, pulmonary and coronary arterial vasodilator in patients with CAD and stable angina pectoris.

Effect of increasing heart rate in patients with aortic regurgitation. Effect of incremental atrial pacing on scintigraphic, hemodynamic and thermodilution measurements.

This study was performed to assess the effect of pacing-induced tachycardia in patients with aortic regurgitation. In 12 patients (5 men and 7 women with a mean age of 53 years) with aortic regurgitation, left ventricular end-diastolic and end-systolic volume indexes were measured with multigated equilibrium blood pool imaging, and forward cardiac index was determined with thermodilution, both at rest (mean heart rate +/- standard deviation 72 +/- 8 beats/min) and during atrial pacing at 100 and 120 beats/min. Pacing caused a decremental reduction in left ventricular end-diastolic and end-systolic volume indexes and radionuclide-determined stroke volume index but no change in radionuclide-determined cardiac index or left ventricular ejection fraction. Forward cardiac index increased incrementally from the baseline value at rest to that at 120 beats/min despite a decremental reduction in stroke volume index. There was a stepwise decrease in regurgitant volume/stroke (46 +/- 20 ml/m2 at baseline, 27 +/- 15 at 120 beats/min; p less than 0.05) but no change in regurgitant volume/min (3.38 +/- 1.80 liters/min per m2 at baseline, 3.22 +/- 1.78 at 120 beats/min; difference not significant [NS]) or regurgitant fraction (0.54 +/- 0.13 at baseline, 0.49 +/- 0.13 at 120 beats/min; NS). Mean femoral arterial, pulmonary arterial and pulmonary capillary wedge pressures did not change with pacing.

Assessment of vasodilator therapy in patients with severe congestive heart failure: limitations of measurements of left ventricular ejection fraction and volumes.

Although noninvasive techniques are often used to assess the effect of vasodilator therapy in patients with congestive heart failure, it is unknown whether changes in noninvasively determined left ventricular ejection fraction, volume, or dimension reliably reflect alterations in intracardiac pressure and flow. Accordingly, we compared the acute effect of sodium nitroprusside on left ventricular volume and ejection fraction (determined scintigraphically) with its effect on intracardiac pressure and forward cardiac index (determined by thermodilution) in 12 patients with severe, chronic congestive heart failure and a markedly dilated left ventricle. Nitroprusside (infused at 1.3 +/- 1.1 [mean +/- standard deviation] microgram/kg/min) caused a decrease in mean systemic arterial, mean pulmonary arterial, and mean pulmonary capillary wedge pressure as well as a concomitant increase in forward cardiac index. Simultaneously, left ventricular end-diastolic and end-systolic volume indexes decreased, but the scintigraphically determined cardiac index did not change significantly. Left ventricular ejection fraction averaged 0.19 +/- 0.05 before nitroprusside administration and increased by less than 0.05 units in response to nitroprusside in 11 of 12 patients. The only significant correlation between scintigraphically and invasively determined variables was that between the percent change in end-diastolic volume index and the percent change in pulmonary capillary wedge pressure (r = 0.68, p = 0.01). Although nitroprusside produced changes in scintigraphically determined left ventricular ejection fraction, end-systolic volume index, and cardiac index, these alterations bore no predictable relation to changes in intracardiac pressure, forward cardiac index, or vascular resistance. Furthermore, nitroprusside produced a considerably greater percent change in the invasively measured variables than in the scintigraphically determined ones.

Efficacy of prazosin in the management of chronic congestive heart failure: a 6-month randomized, double-blind, placebo-controlled study.

The beneficial effects of acute prazosin therapy in patients with congestive heart failure (CHF) have been well documented; however, its chronic efficacy over several months has not previously been evaluated in a placebo-controlled manner. Therefore, an assessment was made by radionuclide ventriculography of the effect of prazosin, 20 mg/day, on left ventricular ejection fraction and end-systolic and end-diastolic volumes at rest and on peak upright bicycle exercise, as well as its effect on right ventricular ejection fraction at rest, exercise time and work load, and standard clinical variables in 23 patients with stable class III symptoms of CHF. The study consisted of a 6-month randomized, double-blind, controlled evaluation of prazosin versus placebo in patients receiving a stable dose of digitalis and diuretics for at least 1 month. At entry, the prazosin and placebo groups did not differ in any respect. Prazosin caused no demonstrable effect on clinical variables such as status of symptoms, heart rate, mean arterial pressure, and cardiothoracic ratio when compared with placebo. Prazosin also caused no demonstrable effect compared with placebo on absolute or percent changes in radionuclide variables at rest or on peak exercise, or on exercise time or exercise work load. In addition, prazosin had no consistent effect compared with placebo on plasma renin activity or plasma catecholamine levels. However, there was a slight but significant increase in weight (p less than 0.0001) and in plasma renin activity in the upright position (p less than 0.002) with time, as well as a tendency for the diuretic dose to increase with time in both groups. Thus, long-term prazosin therapy generally produces no demonstrable subjective or objective improvement in patients with stable, chronic class III CHF receiving digitalis and diuretic therapy.

Assessment of the inotropic and vasodilator effects of amrinone versus isoproterenol.

The hemodynamic effects of graded-dose infusions of amrinone (maximal dose 30 micrograms/kg/min) (10 patients) and isoproterenol (maximum dose 4 micrograms/min) (11 patients) were assessed in patients with a range of left ventricular (LV) function. LV ejection fraction ranged from 0.13 to 0.77 (mean +/- standard deviation 0.47 +/- 0.23) among the patients who received amrinone and from 0.24 to 0.77 (mean 0.52 +/- 0.18) among those who received isoproterenol. Peak-dose amrinone produced a reduction in LV filling pressure (from 15 +/- 10 to 10 +/- 7 mm Hg, p less than 0.001), but no significant change in heart rate, cardiac output, mean aortic pressure, total systemic vascular resistance (TSVR) or LV dP/dt max. In contrast, peak-dose isoproterenol produced a similar reduction in LV filling pressure (from 17 +/- 12 to 13 +/- 13 mm Hg, p less than 0.05), but also caused increases in heart rate, cardiac output and LV dP/dt max and decreases in mean aortic pressure and TSVR (p less than 0.001). The absolute change in cardiac output and stroke volume correlated closely with the change in TSVR in response to amrinone (r = -0.90, p less than 0.001 and r = -0.84, p = 0.002, respectively), but not in response to isoproterenol. Although isoproterenol produced a marked increase in cardiac output and LV dP/dt max (not explained by heart rate changes alone) in all patients, amrinone produced an increase in cardiac output only in those with markedly elevated LV filling pressures (who had a reduction in TSVR), and an increase in LV dP/dt in a minority.

Limitations of qualitative angiographic grading in aortic or mitral regurgitation.

This study was performed to assess the accuracy of qualitative angiographic grading in persons with aortic regurgitation (AR) or mitral regurgitation (MR) and to determine the factors that may influence the reliability of such grading. In 230 patients (152 men, 78 women, aged 52 +/- 14 years) with AR or MR, forward cardiac index was measured by the Fick and indicator dilution techniques and left ventricular (LV) angiographic index by the area-length method, from which the regurgitant volume index was calculated. In 124 other patients (89 men, 35 women, aged 52 +/- 11 years) without regurgitation, there was good agreement between forward and angiographic cardiac indexes (r = 0.87, p less than 0.001). In the 83 patients with AR, the regurgitant volume indexes in those with 1+ (0.87 +/- 0.57 liters/min/m2) and 2+ (1.72 +/- 1.19 liters/min/m2) angiographic regurgitation were not significantly different from one another, but were significantly different from those with 3+ (3.0 +/- 1.42 liters/min/m2) and 4+ (4.80 +/- 2.25 liters/min/m2) regurgitation; at the same time, the regurgitant volume indexes of patients with 3+ and 4+ AR were not significantly different from one another. In the 147 patients with MR, the regurgitant volume indexes in patients with 1+ regurgitation (0.61 +/- 0.64 liters/min/m2) were significantly lower than other grades, but the regurgitant volume indexes of 2+ (1.14 +/- 0.85 liters/min/m2) vs 3+ (2.14 +/- 1.37 liters/min/m2) and of 3+ vs 4+ (4.60 +/- 2.31 liters/min/m2) were not significantly different. With AR and MR, regurgitant flow within each angiographic grade varied widely, especially in grades 3+ and 4+, and there was considerable overlap of regurgitant volume indexes between grades.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of provocation on transcardiac thromboxane in patients with coronary artery disease.

Thromboxane A2 exerts powerful effects on vascular smooth muscle tone and platelet aggregability. Previous studies have demonstrated increases in transcardiac thromboxane B2 (a stable thromboxane A2 metabolite) in patients with unstable angina and recent chest pain. To determine whether these increases in transcardiac thromboxane B2 are unique to the unstable anginal syndrome or are merely a consequence of ongoing myocardial ischemia, simultaneous ascending aortic and coronary sinus blood samples were obtained for quantitation of thromboxane B2 in 52 patients with a history of chest pain. Provocation was performed with (1) rapid cardiac pacing in 23 patients, (2) cold pressor stress in 19 patients, and (3) sustained isometric exertion in 10 patients. Of the 52 patients, only 5 had a substantial (greater than 3-fold) increase in coronary sinus thromboxane B2 in response to provocation: 1 had unstable angina and chest pain during the previous 48 hours and 4 had a myocardial infarction within the previous 6 weeks. Similarly, only 7 had a greater than 3-fold increase in the coronary sinus/aortic thromboxane B2 ratio in response to provocation: 1 had unstable angina and recent chest pain, 5 had a recent myocardial infarction, and 1 had both of these. There were no other clinical features unique to these patients. The remaining patients with similar diagnoses did not develop a marked increase in coronary sinus thromboxane B2 or the coronary sinus/aortic thromboxane B2 ratio with provocation. None of the 35 patients with stable ischemic heart disease or nonischemic chest pain syndromes had a substantial increase in coronary sinus thromboxane B2 or the coronary sinus/aortic thromboxane B2 ratio (p less than 0.001 for both coronary sinus thromboxane B2 and the coronary sinus/aortic thromboxane B2 ratio in comparison with the 17 patients with recent unstable angina or myocardial infarction). Thus, generous amounts of thromboxane B2 are released into the coronary circulation after provocation in some patients with unstable angina or recent myocardial infarction but not in those with stable ischemic heart disease or nonischemic chest pain syndromes.

Effect of selective coronary arteriography on left ventricular volumes and ejection fraction in man.

This study was performed to assess the influence of selective coronary arteriography on left ventricular volumes and ejection fraction in man. In 30 patients with assorted cardiac diseases, left ventricular end-diastolic and end-systolic volumes and ejection fraction were quantitated immediately before and after selective coronary arteriography. In 19 patients (Group A), contrast left ventriculography was performed immediately before and after selective coronary arteriography. In the remaining 11 patients (Group B), multigated equilibrium blood pool imaging was performed just before and after coronary arteriography. In both groups, mean systemic arterial pressure and heart rate did not change from just before the first to immediately before the second assessment of left ventricular volumes and ejection fraction, but left ventricular end-diastolic pressure increased. End-diastolic and end-systolic volume indexes, and ejection fraction did not change from just before to immediately after selective coronary arteriography. Therefore, selective coronary arteriography (1) consistently causes an increase in left ventricular end-diastolic pressure but (2) exerts no effect on left ventricular volumes and ejection fraction, even in patients with severely compromised left ventricular function.

Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia.

Atrial pacing has been used to assess the physiologic impact of coronary artery disease (CAD). Several variables have served as markers of pacing-induced myocardial ischemia, but their specificities and sensitivities are unknown. Accordingly, in 28 patients, incremental atrial pacing was performed. Of the 28, 10 had no CAD. The left ventricular ejection fraction (LVEF) (by gated equilibrium blood pool scintigraphy) increased in this group (0.60 +/- 0.11 [mean +/- standard deviation] before pacing to 0.67 +/- 0.13 at peak-pacing, p = 0.002). In no patient did left ventricular end-diastolic pressure increase by greater than 5 mm Hg. No patient had lactate production, and 2 (20%) had electrocardiographic S-T segment depression greater than or equal to 0.1 mV. Four (40%) had chest pain with atrial pacing. In the remaining 18 patients with CAD, atrial pacing caused a decrease in LVEF greater than or equal to 0.05 (0.46 +/- 0.10 to 0.33 +/- 0.09, p less than 0.001) and new segmental wall motion abnormalities in all, indicating pacing-induced myocardial ischemia. Only 8 (44%) had an increase in left ventricular end-diastolic pressure of greater than 5 mm Hg, and only 9 (50%) had lactate production. Ten (56%) had ischemic electrocardiographic changes, and 12 (67%) had chest pain. Thus, the electrocardiographic, metabolic, and hemodynamic alterations that may accompany pacing-induced ischemia are specific but relatively insensitive markers of ischemia. In contrast, chest pain during atrial pacing is a nonspecific occurrence, appearing with similar frequency in normal subjects and patients with CAD and pacing-induced ischemia.