Nuclear cardiology after angioplasty and stent placement: beyond sensitivity and specificity.
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Adult↗
Biomedical subjects
D E Manyari
Publications and source records attributed to D E Manyari.
Vascular and cardiac effects of amlodipine in acute heart failure in dogs.
BACKGROUND: Amlodipine improves exercise capacity in patients with chronic congestive heart failure (HF), but the mechanisms of this effect are unknown. OBJECTIVE: To test the hypothesis, in a canine model of acute, ischemic HF, that amlodipine increases vascular capacitance and reduces cardiac filling pressures. METHODS: Amlodipine was given to 13 anesthetized, splenectomized dogs (six controls and seven with HF). Aortic, left ventricular end-diastolic (LVEDP) and portal venous (Pportal) pressures, cardiac output, portal flow (ultrasonic probe) and intestinal blood volume (IBV, 99mTc blood-pool scintigraphy) were measured. Intestinal vascular conductance (= 1/resistance) and vascular capacitance (CAP) were measured before and 15 mins after repetitive 150 micrograms/kg dosages of amlodipine (maximum cumulative dosage, 1000 micrograms/kg). Pportal-IBV curves were obtained by impeding portal flow (pneumatic cuff), and change in CAP was defined by the change in IBV at Pportal = 7.5 mmHg. HF was induced by microsphere embolization of the left coronary artery. RESULTS: CAP increased in the control group (+ 28%, P < 0.01) but decreased (-9%, P < 0.05) in the HF group. Left ventricular stroke work increased in the control group (P < 0.05), while it decreased (P < 0.05) in the HF group, suggesting a negative inotropic effect. In the control group, LVEDP increased after amlodipine was given (P < 0.05) but did not change significantly in the HF group. CONCLUSIONS: In the acute experimental HF model, amlodipine failed to increase intestinal vascular CAP or decrease filling pressures, and may have had a negative inotropic effect. The experiment failed to demonstrate a beneficial hemodynamic effect of amlodipine in acute HF, and the mechanism of benefit of this agent in chronic HF remains unclear.
Acute Disease↗
Limitations of 'personal formularies'.
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Formularies as Topic↗
Cardiac vagal reflex modulates intestinal vascular capacitance and ventricular preload in anesthetized dogs with acute myocardial infarction.
BACKGROUND: The purpose of the present study was to examine the effects of the cardiac vagal reflex on intestinal vascular capacitance and cardiac filling pressure during experimental acute myocardial infarction (AMI). METHODS AND RESULTS: AMI was induced in anesthetized dogs through injection of microspheres into the left main coronary artery. Intestinal blood volume was measured with blood-pool scintigraphy. Portal venous pressure was varied through graded inflation of a portal venous constrictor to determine the intestinal vascular pressure-volume relation. Induction of AMI decreased intestinal blood volume to 88 +/- 3% of the control value (P < .01) and shifted the pressure-volume relation toward the pressure axis. This change was associated with increased left ventricular (LV) end-diastolic pressure (LVEDP) (from 6 +/- 1 to 17 +/- 2 mm Hg, P < .01) and LV segment length (to 112 +/- 4% of the control value, P < .01). During AMI, blockade of the cardiac vagal reflex by intrapericardial application of 2% lidocaine further decreased intestinal blood volume (to 83 +/- 3% of the control value, P < .05, versus AMI without lidocaine), increased LVEDP (to 22 +/- 2 mm Hg, P < .05, versus AMI without lidocaine), and tended to increase LV segment length (to 115 +/- 5%, P < .10). Lidocaine had no effect in dogs with AMI that had been vagotomized. CONCLUSIONS: These results suggest that the cardiac vagal reflex modulates the decrease in the intestinal vascular capacitance induced by AMI and modulates ventricular preload through pooling of blood in the intestinal circulation.
Animals↗
Abnormal reflex venous function in patients with neuromediated syncope.
OBJECTIVES: We sought to compare the forearm reflex venous response to mental arithmetic stress in patients with neuromediated syncope and in normal subjects. BACKGROUND: Patients 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. METHODS: Twelve 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. RESULTS: During 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. CONCLUSIONS: Patients 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.
Adult↗
Ventricular interaction and venous capacitance modulate left ventricular preload.
The concept of left ventricular (LV) 'preload' has seemed simple and straightforward. Similarly, the capacitance function of the veins seemed to be defined, in spite of the fact that 'venous return' might be said to be increased in heart failure when it was obvious that cardiac output was substantially decreased. In studies during the past several years, we have demonstrated that pericardial pressure, as a major modulator of ventricular interaction, must be accounted for before preload, myocardial compliance or contractility can be assessed reliably. Also, using a new conceptual model based on venous pressure-volume relations that explains how changes in venous capacitance modulate ventricular preload, we have defined the comparative capacitance-conductance effects of various vasodilators in a model of heart failure. We conclude that left ventricular preload is significantly modulated by both changes in ventricular interaction and venous capacitance. To optimize the care of patients with heart disease, it is important to understand both these mechanisms.
Heart Failure↗
Nifedipine in severe aortic regurgitation.
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Aortic Valve Insufficiency↗
Splanchnic venous pressure-volume relation during experimental acute ischemic heart failure. Differential effects of hydralazine, enalaprilat, and nitroglycerin.
BACKGROUND: Vasodilator 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. METHODS AND RESULTS: Experimental 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). CONCLUSIONS: Acute 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.
Animals↗
Measurement of intestinal vascular capacitance in dogs: an application of blood pool scintigraphy.
To define relative changes in intestinal vascular capacitance, we developed a model that allowed us to construct intestinal vascular pressure-volume relationships (PVR). Thirteen alpha-chloralose-anesthetized and splenectomized dogs were studied using a pneumatic constrictor and a small catheter to change and measure portal venous pressure. A small lead sheet was placed beneath the abdominal wall. Relative changes in intestinal blood volume (IBV) were determined by in vivo blood pool scintigraphy with 99mTc-labeled erythrocytes and were expressed as percentages corrected for specific activity and abdominal wall radioactivity. PVRs were constructed using data recorded during graded inflations of the portal venous constrictor. The abdominal wall contributed 32.4 +/- 7.7% (SD) of the total counts. During a 4-h control period, PVRs varied by no more than 6% (of IBV). In the isolated intestinal circulation, the change in IBV was precisely proportional to the volume of blood added, indicating that this method can detect very small changes in volume (< or = 5 ml). Nitroglycerin (25 micrograms.kg-1.min-1) increased capacitance by 20%. Although it measures only relative changes, the model is stable and sensitive, provides reproducible measurement of intestinal PVRs, and, with adaptation, may prove useful in patient studies.
Abdomen↗
The veins and ventricular preload.
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Blood Circulation↗
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.
Erythrocytes↗
The effect of nitroglycerin on pulmonary vascular capacitance in dogs.
In this study we investigated the hypothesis that the decrease in pulmonary vascular pressures observed after administration of nitroglycerin is in part due to a shift in the pulmonary vascular pressure-volume relationship. The experiments were done in six closed-chest dogs anesthetized with pentobarbital, in which pulmonary, cardiac, and intestinal relative blood volumes were determined by equilibrium blood pool scintigraphy. Nitroglycerin (30 micrograms/kg/min) caused 7% (p less than 0.02) and 12% (p less than 0.02) reductions in pulmonary and total cardiac blood volume, respectively, and a 7% (p less than 0.01) increase in intestinal blood volume. This shift of blood from the heart and the pulmonary circulation to the systemic (intestinal) circulation was accompanied by reductions in mean pulmonary artery pressure from 16 +/- 2 mm Hg to 12 +/- 1 mm Hg (p less than 0.01), in mean pulmonary capillary wedge pressure from 11 +/- 2 mm Hg to 6 +/- 1 mm Hg (p less than 0.01), and in mean portal pressure from 9 +/- 1 mm Hg to 8 +/- 1 mm Hg (p less than 0.01). The position of the pulmonary vascular pressure-blood volume relationship was unaffected by nitroglycerin, whereas the portal pressure-intestinal blood volume relationship was shifted to the left and upward. These changes suggest that pulmonary vascular tone remained unchanged, whereas intestinal vascular tone decreased during administration of nitroglycerin. In conclusion, nitroglycerin decreased pulmonary vascular pressures through a passive emptying of the pulmonary circulation as a result of increased systemic (intestinal) vascular capacitance.
Animals↗
Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study.
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Cardiomegaly↗
Atrial and ventricular arrhythmias in asymptomatic active elderly subjects: correlation with left atrial size and left ventricular mass.
Elderly normal subjects have an increased prevalence of cardiac arrhythmias compared with young and middle-aged subjects. The objective of this study was to test the hypothesis that the incidence and complexity of atrial and ventricular arrhythmias may be related to either left atrial enlargement or to increased left ventricular mass, respectively. From 146 asymptomatic volunteers older than 60 years, 86 subjects were considered to be free of cardiovascular abnormalities and had adequate M-mode echocardiograms and 24-hour ambulatory electrocardiograms. The mean age was 72 +/- 7 years, with a range of 60 to 96 years. There were 37 men and 49 women. During 1415 +/- 73 minutes of ambulatory electrocardiography, the average heart rate was 72 +/- 8 beats/min in men and 76 +/- 6 beats/min in women (p less than 0.05). Atrial arrhythmias were present in 64 subjects (74%); the frequency and complexity of these arrhythmias correlated with left atrial size (p less than 0.01). Ventricular arrhythmias were present in 55 subjects (64%); the frequency and complexity of ventricular arrhythmias did not correlate with left ventricular mass index. These results suggest that left atrial dilatation, a normal development in healthy elderly subjects, plays a significant role in the pathophysiology of the increased incidence of atrial arrhythmias. Increased left ventricular mass, which also occurs normally in the aging heart, is not, on the other hand, associated with an increased frequency and/or complexity of ventricular arrhythmias.
Aged↗
Melperone: electrophysiologic and antiarrhythmic activity in humans.
Previous studies in animals and in humans have shown that melperone, a neuroleptic butyrophenone, has class III electrophysiologic activity. However, its antiarrhythmic activity has not been assessed in humans. Accordingly, the electrophysiologic and antiarrhythmic effects of melperone were assessed in 23 patients with symptomatic ventricular tachyarrhythmias. Seventeen patients had electrophysiologic testing while receiving melperone. At oral daily dosages greater than or equal to 240 mg, melperone produced significant prolongations of QT intervals (385 +/- 11 vs. 355 +/- 22 ms, p less than 0.05), ventricular effective refractory periods (263 +/- 18 vs. 243 +/- 28 ms, p less than 0.05; 260 +/- 18 vs. 235 +/- 27 ms, p less than 0.01; and 243 +/- 23 vs. 222 +/- 28 ms, p less than 0.01; at 600-, 500-, and 400-ms pacing cycle lengths, respectively) and ventricular tachycardia (VT) cycle lengths (286 +/- 46 vs. 239 +/- 70 ms, p less than 0.05). Inducible VT was suppressed entirely in one patient. In three other patients, inducible sustained VT became nonsustained. No significant negative inotropic effects were observed. The majority of patients (70%) experienced some adverse effect, the commonest of which was neurologic. In conclusion, melperone had significant class III electrophysiologic and antiarrhythmic activity in humans. Its clinical use may be limited by the high incidence of adverse effects.
Adult↗
Assessment of the splanchnic vascular capacity and capacitance using quantitative equilibrium blood-pool scintigraphy.
A series of human and animal experiments were carried out to assess the usefulness of equilibrium blood pool scintigraphy (EBPS) to study acute changes of the splanchnic vascular capacity and the splanchnic vascular pressure-volume (P-V) relationship. Corrected regional abdominal count rate changes, before and after various pharmacologic interventions, were used to assess regional splanchnic vascular volume changes. Animals were instrumented to manipulate and record splanchnic venous pressures. In patients, splanchnic vascular capacity increased by 5.2 +/- 6.9% (p less than 0.001) after 0.6 mg sublingual nitroglycerin while no significant change was noted after sugar pills (0.9 +/- 5.2%, p greater than 0.3). In dogs, splanchnic vascular capacity decreased by a mean of 16% during infusion of angiotensin (p less than 0.001) and increased by a mean of 32% during infusion of nitroprusside (p less than 0.001). The splanchnic vascular P-V curve was shifted rightwards during nitroglycerin administration. Thus, using the radionuclide technique we detected the expected qualitative and quantitative shifts in splanchnic capacity and capacitance. We conclude that EBPS is a useful method to assess acute changes of 1) the splanchnic vascular P-V relationship, in invasive animal studies, and 2) the splanchnic vascular capacity in noninvasive human and animal studies.
Adult↗
Importance of effective, early and sustained reperfusion during acute myocardial infarction.
The determinants of myocardial salvage after thrombolytic therapy during acute myocardial infarction (AMI) have not been clearly defined. In 1984, a prospective randomized trial was undertaken to define the relations between delay to treatment and effectiveness of perfusion to salvage of myocardium. Patients presenting within 2 hours of symptom onset received intravenous streptokinase immediately (group 1, 20 patients) or 5 hours after symptom onset (group 2, 16 patients). Effective perfusion (less than or equal to 90% residual stenosis with rapid distal runoff) occurred in 63% of patients in both groups. Five patients, all in group 1, had recurrent AMI; 4 of the 5 had effective perfusion. There was no group difference in left ventricular ejection fraction at baseline or before discharge. However, group 1 patients with effective perfusion tended to have a greater predischarge mean ejection fraction than those in group 1 with ineffective perfusion (53 +/- 13 vs 44 +/- 16%, p less than 0.10) and had a greater mean value than those in group 2 with ineffective perfusion (53 +/- 13 vs 38 +/- 17%, p less than 0.03). The ejection fraction did not change significantly between admission and discharge in either group, but it increased significantly in group 1 patients with effective perfusion and no recurrent AMI (delta EF = +6 +/- 8%, p less than 0.04). Group 1 patients with ineffective perfusion had a significant decrease in ejection fraction (delta EF = -4 +/- 4%, p less than 0.04). In group 2 patients the ejection fraction did not change, regardless of the state of perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Is the residual translesional pressure gradient useful to predict regional myocardial perfusion after percutaneous transluminal coronary angioplasty?
Routine assessment of the severity of a coronary artery lesion with coronary cineangiography is limited by its variability and poor correlation with blood flow and postmortem findings. In this investigation, we compared the usefulness of the final coronary artery translesional pressure gradient and the final angiographic coronary percent stenosis to assess immediate percutaneous transluminal coronary angioplasty (PTCA) success. To accomplish this, pressure gradients and percent stenoses were compared to stress thallium-201 regional myocardial perfusion before and after 56 uncomplicated PTCAs in 51 patients with single-vessel coronary artery disease. There were 39 men and 12 women; their mean age was 59 +/- 12 years. No patient had evidence of myocardial infarction. A new quantitative method to assess regional myocardial perfusion was used. Patients exercised for 433 +/- 130 seconds before PTCA and for 545 +/- 126 seconds after PTCA (p less than 0.001). Group coronary stenosis and translesional pressure gradient decreased from 77 +/- 11% and 48 +/- 5 mm Hg, respectively, before PTCA, to 25 +/- 11% and 9 +/- 5 mm Hg, respectively, after PTCA (p less than 0.001). Regional myocardial perfusion in the segment of the diseased (dilated) coronary artery increased after PTCA from 77 +/- 17% to 94 +/- 9% (p less than 0.001). Although a significant relationship was noted between regional myocardial perfusion and percent stenosis and translesional pressure gradient, a large individual scatter was present (r values lower than 0.55). We conclude that the final translesional pressure gradient during PTCA is not a better measure of immediate PTCA success than the angiographic percent stenosis.
Adult↗