Dante E. Manyari

Sequential thallium-201 myocardial perfusion studies after successful percutaneous transluminal coronary artery angioplasty: delayed resolution of exercise-induced scintigraphic abnormalities.

To characterize the sequential changes of myocardial perfusion scintigraphy in patients with coronary artery disease (CAD) after complete revascularization, 43 patients underwent exercise thallium-201 (201Tl) myocardial perfusion scintigraphy before and at 9 +/- 5 days, 3.3 +/- 0.6, and 6.8 +/- 1.2 months after percutaneous transluminal coronary angioplasty (PTCA). Only patients with single-vessel CAD, without previous myocardial infarction, and without evidence of restenosis at 6 to 9 months after PTCA were included. Perfusion scans were analyzed blindly with the use of a new quantitative method to define regional myocardial perfusion in the topographic distribution of each coronary artery, which was shown to be reproducible (r = .94 or higher and SEE of 7% or less, between repeated measures by one and two operators). At 4 to 18 days after PTCA, the mean treadmill walking time increased by 123 +/- 42 sec, mean exercise-induced ST segment depression decreased by 0.6 +/- 0.3 mm, group maximal heart rate increased by 20 +/- 9 beats/min, and group systolic blood pressure at peak exercise increased by 24 +/- 10 mm Hg, compared with pre-PTCA values (p less than .001). However, no group differences were noted in these variables between the three post-PTCA stages. Myocardial perfusion in the distribution of the affected (dilated) coronary artery, on the other hand, improved progressively. In the 45 degree left anterior oblique view for instance, myocardial perfusion increased at 9 days after PTCA (from 68 +/- 24% before PTCA to 91 +/- 9%, p less than .001) and at 3.3 months after PTCA (101 +/- 8%, p less than .05 vs 9 days after PTCA), but no further significant changes were seen at 6.8 months after PTCA (102 +/- 8%). Similar changes were noted in the other two views. No relationship between minor complications during PTCA and delayed improvement on the 201Tl was observed. Myocardial ischemia was diagnosed in 12 of the 43 scans recorded a few days after PTCA, but in none recorded at later stages. We conclude that 201Tl scans after PTCA often show delayed improvement and therefore, an abnormal myocardial perfusion scan soon after PTCA does not necessarily reflect residual coronary stenosis or recurrence.

Abnormal reflex venous function in patients with neuromediated syncope

OBJECTIVESnWe sought to compare the forearm reflex venous response to mental arithmetic stress in patients with neuromediated syncope and in normal subjects.nnnBACKGROUNDnPatients with neuromediated syncope have a paradoxic arterial vasodilation in response to stressors that usually provoke vasoconstriction. Given the postulated role of diminished preload in provoking the reflex responses resulting in syncope, we hypothesized that mental stress might provoke paradoxic reflex venodilation in patients with neuromediated syncope.nnnMETHODSnTwelve normal subjects (mean age [+/-SD] 47 +/- 9 years) and 27 patients with neuromediated syncope (mean age 42 +/- 13 years) were studied before and during a mental arithmetic stress test. Forearm venous pressure-volume relations were determined by using radionuclide plethysmography.nnnRESULTSnDuring mental arithmetic stress, heart rate and systolic and diastolic blood pressure increased significantly and similarly both in normal subjects and in patients with neuromediated syncope. The heart rate and blood pressure changes were qualitatively similar in both groups. However, with mental arithmetic stress, forearm venoconstriction of 13 +/- 2% (mean +/- SEM) was noted in normal subjects (p < 0.001) but not in patients with neuromediated syncope (mean 2%, p = NS). This group response of patients with neuromediated syncope did not result from a lack of individual responses but occurred because these patients had a wide range of responses. The normal physiologic and methodologic variability of the method was +/- 4%. Thirteen of the 27 patients with neuromediated syncope had forearm venoconstriction of 14.5 +/- 6.8% during mental arithmetic stress, whereas 7 had paradoxic forearm venodilation of 14.6 +/- 8.8%, and 7 were considered nonresponders (-1.3 +/- 3.4%). Thus, 14 (52%) of the 27 patients with syncope did not have normal vasoconstriction in response to mental stress.nnnCONCLUSIONSnPatients with neuromediated syncope have an abnormal range of forearm venomotor responses to mental arithmetic stress. Reflex control of the veins may play an important role in the pathogenesis of neuromediated syncope.

Comparative value of the cold-pressor test and supine bicycle exercise to detect subjects with coronary artery disease using radionuclide ventriculography.

Left ventricular ejection fraction (EF) and wall motion studies were performed using blood pool cardiac scintigraphy before and during the cold-pressor test (CPT) and bicycle exercise. Twenty normal subjects responded to the CPT with no change or a significant increase (7% or more) of the EF and no new wall motion abnormalities. Mean EF increased significantly (p < 0.01). Two subjects responded abnormally to the CPT, one with a significant decrease (7% or more) in EF and another with the development of new wall motion abnormalities. During exercise, EF increased significantly in all-but one subject (p < 0.001). No new wall motion abnormality was seen. In 20 patients with coronary artery disease (CAD) and normal resting left ventricular function, mean EF decreased (p < 0.001) during the CPT, but only 11 patients could be identified individually by a drop in EF of 7% or more. During exercise, 18 of the 20 patients responded abnormally (failure to increase EF by 7% or more). Twelve patients showed new wall motion abnormalities during CPT and 15 during exercise. Three patients during the CPT and one during exercise had normal EF response while developing new wall motion abnormalities. Thus, the sensitivity of radionuclide EF changes during the CPT to detect subjects with CAD was 55%. It increased to 70% when wall motion analysis and EF changes were considered. The specificity was then 90% and the predictive accuracy was 88%. The sensitivity of radionuclide studies during exercise, considering EF changes and wall motion analysis under otherwise similar conditions, was 95%. Specificity and predictive accuracy were also 95%. We conclude that the CPT is not as sensitive as exercise for detecting subjects with CAD by radionuclide cardiac angiography. The CPT may be a useful intervention in subjects in whom adequate exercise cannot be accomplished.

Isosorbide dinitrate and glyceryl trinitrate: Demonstration of cross tolerance in the capacitance vessels☆

Cross tolerance to the arterial effects of sublingual glyceryl trinitrate (GTN) has been demonstrated in subjects taking oral isosorbide dinitrate (ISDN). To determine if cross tolerance also develops in the venous system, the effects of 0.6 mg of GTN on venous capacitance were assessed before (stage A) and during (stage B) therapy with ISDN. Venous capacitance was assessed using the radionuclide blood pool method, with relative changes in regional blood volume measured in the forearm in 6 patients and the splanchnic circulation in 4 patients. Heart rate, blood pressure and blood volume were measured before and at 1-minute intervals for 10 minutes after GTN; there was less than 2% variability in regional blood volume during 6 control measurements. During stage A, 5 minutes after GTN, systolic blood pressure (mean +/- standard deviation) decreased by 14% (from 125 +/- 15 to 107 +/- 19 mm Hg, p less than 0.01) and heart rate increased by 17% (from 68 +/- 14 to 80 +/- 17 beats/min, p less than 0.001), while regional blood volume increased to 101 +/- 2% at 1 minute (difference not significant [NS]), 111 +/- 2% at 5 minutes (p less than 0.001) and 107 +/- 3% at 10 minutes (p less than 0.01) relative to baseline measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of the human splanchnic venous volume-pressure relation using radionuclide plethysmography. Effect of nitroglycerin.

Background. No method exists to assess human splanchnic venous function, the most important region in terms of vascular capacity. Methods and Results. We studied 25 stable patients without heart failure or hypertension to develop a method to assess the splanchnic venous volume‐pressure (V‐P) relation and to determine the effect of nitroglycerin (GTN). We used blood pool scintigraphy to assess changes in regional splanchnic vascular volume (SVV) and low levels of continuous positive airway pressure (CPAP) to passively alter venous pressure and thus, SVV. We postulated that the relation between SVV and the CPAP used would reflect the capacitance of the splanchnic venous bed and that changes in the position of this relation would provide a relative measurement of any change in capacitance. In 12 patients (group 1), the splanchnic vascular V‐P curves were recorded before and 2, 9, and 20 minutes after 0.6 mg sublingual GTN; in eight patients (group 2), recordings were made at similar times before and after sublingual administration of placebo; in five patients (group 3), the hemodynamic effects of CPAP were assessed by means of right and left cardiac catheterization. Right atrial and femoral venous pressures increased (p < 0.001) and cardiac output fell (p < 0.05) during CPAP. There was an apparently linear relation between CPAP and SVV (r=0.74‐0.98); SVV increased an average of 7.4±2.2% (p<0.001) by 12 cm H2O CPAP. The splanchnic vascular V‐P curves were reproducible with minimal variability in SVV (±2%, p>0.2) in group 2. After administration of GTN, the splanchnic vascular V‐P curve shifted away from the pressure axis in a parallel fashion by an average of 9.4±5.4% (p<0.001). Conclusions. We have developed a reproducible noninvasive technique that may be used to assess human splanchnic venous V‐P relations. We have demonstrated for the first time in humans that GTN exerts its dilatory effect by increasing the unstressed splanchnic venous volume. (Circulation 1993;87:1142‐1151)

Volume-pressure analysis of reflex changes in forearm venous function. A method by mental arithmetic stress and radionuclide plethysmography.

Mental arithmetic stress is known to cause forearm arterial dilation, but the venous responses, including possible changes in the volume-pressure relation, have not been defined. Hence, 10 apparently normal subjects, eight men and two women, mean age 46 +/- 9 years, were studied before and during mental arithmetic stress. Changes in forearm venous volume were estimated with 99mTc blood pool scintigraphy. Group variability of this measurement technique was 1.8 +/- 2.3%. A brachial blood pressure cuff was used to obtain venous occluding pressures of 0, 10, 20, and 30 mm Hg. Mental arithmetic stress increased group systolic and diastolic blood pressure from 126 +/- 12 to 152 +/- 20 mm Hg and from 83 +/- 8 to 93 +/- 15 mm Hg, respectively (p less than 0.001). Heart rate increased from a mean of 75 +/- 15 to 85 +/- 17 beats/min (p less than 0.01). There was no evidence of interaction between or nonlinearity of the volume-pressure plots. Linear regression then yielded the equations V = 99.8 + 0.96P before and V = 86.3 + 0.96P during mental arithmetic stress, which represents a 13.5 +/- 1.6% decrease in forearm vascular volume (p less than 0.001). We conclude that 1) a linear relation exists between forearm venous volume and pressure at physiologic pressures before and during mental arithmetic stress; 2) mental arithmetic stress causes forearm venoconstriction; and 3) such venoconstriction takes place by a parallel shift in the volume-pressure relation (i.e., a shift in unstressed venous volume).

Assessment of pericardial constraint: The relation between right ventricular filling pressure and pericardial pressure measured after pericardiocentesis

Experimental studies have shown that right ventricular filling pressure (that is, intracavitary diastolic pressure) approximates pericardial surface pressure but, in many patients after removal of pericardial effusion, right ventricular filling pressure has been found to markedly exceed pericardial pressure recorded by an open catheter. The aim of this study was to determine whether this apparent contradiction was related to the technique of pericardial pressure measurement. Nine patients with chronic pericardial effusion were studied and, although these pressures diverged to varying degrees in individual patients, the previous observation was confirmed in that, although initially similar, right ventricular filling pressure and pericardial pressure (measured by means of an open catheter) tended to diverge during removal of the effusate; when the evacuation was as complete as possible pericardial pressure was 2.1 +/- 1.0 (mean +/- SE), while right ventricular filling pressure was 8.7 +/- 1.7 mm Hg (p less than 0.01). In six open chest, anesthetized, volume-loaded dogs with pericardial effusion (50 ml), right ventricular filling pressure and pericardial pressures measured with both open catheter and flat balloon were all equal. With decreasing volume of pericardial fluid, right ventricular filling pressure and pericardial pressure (by catheter) diverged as had been observed in patients. However, pericardial pressure (balloon) continued to be equal to right ventricular filling pressure. (With 0 ml in the pericardium, right ventricular filling pressure = 12.9 +/- 0.9 mm Hg, pericardial pressure [catheter] = 1.4 +/- 1.9 mm Hg and pericardial pressure [balloon] = 12.4 +/- 1.5 mm Hg.) Thus, these observations support the use of right ventricular filling pressure as an estimate of pericardial constraint in patients.

Splanchnic Venous Pressure–Volume Relation During Experimental Acute Ischemic Heart Failure Differential Effects of Hydralazine, Enalaprilat, and Nitroglycerin

BACKGROUNDnVasodilator drugs have variable effects on veins and arteries. However, direct measurements of their effects on the splanchnic veins, perhaps the most important volume reservoir, have not been reported. We assessed the effect of acute heart failure and the subsequent administration of hydralazine, enalaprilat, and nitroglycerin on the splanchnic venous pressure-volume relation in intact dogs.nnnMETHODS AND RESULTSnExperimental acute ischemic heart failure was induced in 19 splenectomized dogs by microsphere embolization of the left main coronary artery. Embolization was repeated until left ventricular end-diastolic pressure (LVEDP) reached 20 mm Hg and cardiac output decreased by 50%. The splanchnic vascular pressure-volume relation was determined by radionuclide plethysmography during the control stage, after acute heart failure had been established, and after administration of a vasodilator (hydralazine, enalaprilat, or nitroglycerin) at a dose sufficient to reduce mean aortic pressure by approximately 20%. Induction of acute heart failure was associated with a decrease in the splanchnic vascular volume from 100% to 86 +/- 2% and an increase in LVEDP from 6 +/- 1 to 21 +/- 1 mm Hg (P < .001). There was a parallel leftward shift of the splanchnic vascular pressure-volume curve. After the administration of hydralazine, enalaprilat, and nitroglycerin, the splanchnic vascular volumes increased from 86% to 88 +/- 3%, 96 +/- 3%, and 113 +/- 3%, respectively (P = NS, P < .01, and P < .001, respectively, versus heart failure). After drug administration, the LVEDPs were 18 +/- 2, 16 +/- 1, and 13 +/- 1 mm Hg (P = NS, P < .05, and P < .001, respectively, versus heart failure).nnnCONCLUSIONSnAcute heart failure was associated with a parallel leftward shift of the splanchnic venous pressure-volume relation (venoconstriction). Splanchnic (systemic) venoconstriction may in part explain the increased LVEDP during acute heart failure by displacement of blood to the central compartment. Subsequently administered enalaprilat and, to a greater degree, nitroglycerin produced splanchnic venodilation, thereby lowering LVEDP. Hydralazine had no significant effect on the splanchnic veins and only a modest effect on LVEDP. In this model, splanchnic capacitance changes appear to modulate change in left ventricular preload.

Effect of Pericardiocentesis on Right and Left Ventricular Function and Volumes in Pericardial Effusion

To assess the effects of pericardial effusion on ventricular performance and volumes, electrocardiographically gated blood pool cardiac scintigraphy was performed immediately before and after 14 pericardiocenteses in 10 patients, 7 men and 3 women, aged 28 to 73 years (mean 50). Cardiac tamponade was present in 5 patients. After removal of 140 to 1,100 ml of pericardial fluid (527 +/- 305 ml [mean +/- standard deviation]), left ventricular (LV) ejection fraction increased from 63 +/- 5 to 64 +/- 4% (p greater than 0.05) and right ventricular (RV) ejection fraction decreased from 47 +/- 4 to 46 +/- 2% (p greater than 0.05). LV end-diastolic and end-systolic volumes increased (p less than 0.01) by 28 and 33%, and RV volumes by 40 and 43%, respectively. There were 8 patients with normal LV function (ejection fraction greater than 60%) and 6 patients with subnormal LV function. Changes in ejection fraction were nonsignificant in the 4 subgroups. LV end-diastolic volume changes were more marked (p less than 0.01) in patients with cardiac tamponade (+ 56%) than in those without tamponade (+ 17%), and in those with normal LV function (+ 36%) than in those with subnormal LV function (+ 21%). RV end-diastolic volume increased more markedly (p less than 0.05) in patients with tamponade (+ 72%) than in those without tamponade (+ 23%), but were similar in patients with normal (+ 38%) and abnormal (+ 43%) LV function. After pericardiocentesis, RV volume increased more markedly than did LV volume. Thus, hemodynamic and clinical improvement after pericardiocentesis may be related only to an increase in stroke volume. RV and LV ejection fraction, a measure of myocardial contractility, was not affected significantly by the presence of pericardial effusion, even in those patients who had cardiac tamponade.

Modulation of vascular capacitance by angiotensin and nitroprusside: a mechanism of changes in pericardial pressure.

The aim of the present study was to test the hypothesis that vasoactive drugs may modify left ventricular diastolic function by shifting blood between the systemic vascular bed and the heart, thereby changing pericardial and left ventricular pressure. The experiments were done in 10 open-chest, anesthetized, previously splenectomized dogs in which changes in pericardial surface pressure in response to intravenous sodium nitroprusside and angiotensin were related to changes in blood volume in the abdominal region. Blood volume was determined by blood pool scintigraphy (99mTc) and regions of interest were drawn in the liver and in the mesenteric area. Angiotensin was infused at rates that were adjusted to increase mean aortic pressure by 20 and 30 mm Hg, and nitroprusside was infused at rates to decrease mean aortic pressure by 30 and 50 mm Hg. Angiotensin increased pericardial pressure by 3 and 5 mm Hg at the respective doses and there were increments in left ventricular end-diastolic pressure (LVEDP) and left ventricular diameter (sonomicrometry). Angiotensin decreased blood volume in the mesenteric region by 14% and 17%, but did not significantly change blood volume in the liver region. Angiotensin increased portal venous pressure and decreased mesenteric blood volume, suggesting decreased mesenteric venous compliance. Nitroprusside had opposite effects: pericardial pressure was decreased by 5.5 and 6.5 mm Hg by the respective doses. The doses of nitroprusside increased blood volume in the mesenteric region by 14% and 20%, but did not significantly change blood volume in the liver region.(ABSTRACT TRUNCATED AT 250 WORDS)