Effects of intraaortic balloon pumping on septal arterial blood flow velocity waveform during severe left main coronary artery stenosis

OBJECTIVES: We sought to evaluate the effect of intraaortic balloon pumping on the phasic blood velocity waveform into myocardium with severe coronary artery stenosis. BACKGROUND: In the presence of severe coronary artery stenosis, it is not clear whether intraaortic balloon pumping augments intramyocardial inflow during diastole or changes systolic retrograde blood flow from the myocardium to the extramural coronary arteries. METHODS: Using anesthetized open chest dogs (n=7), we introduced severe stenosis in the left main coronary artery to reduce the poststenotic pressure to approximately 60 mm Hg (>90% diameter stenosis). Septal arterial blood flow velocities were measured with a 20-MHz, 80-channel ultrasound pulsed Doppler velocimeter. Left anterior descending arterial flow, aortic pressure and poststenotic distal coronary pressure were measured simultaneously. The diastolic anterograde flow integral and systolic retrograde flow integral were compared in the presence and absence of intraaortic balloon pumping. RESULTS: Although intraaortic balloon pumping augmented diastolic aortic pressure, this pressure increase was not effectively transmitted through stenosis. Septal arterial diastolic flow velocity was not augmented, and left anterior descending arterial flow was unchanged during intraaortic balloon pumping. CONCLUSIONS: In the presence of severe coronary artery stenosis, intraaortic balloon pumping failed to increase diastolic inflow in the myocardium and did not enhance systolic retrograde flow from the myocardium to the extramural coronary artery. Thus, the major effect of intraaortic balloon pumping on the ischemic heart with severe coronary artery stenosis may be achieved by reducing oxygen demand by systolic unloading.     

Clinical, biological, and immunophenotypical characteristics of B-cell chronic lymphocytic leukemia with trisomy 12 by fluorescence in situ hybridization

Intra-aortic balloon pumping is frequently used in patients with cardiogenic shock when oliguria persists despite maximal pharmacologic support. The objective of this study was to measure the effect of intra-aortic balloon pumping on renal blood flow, renal oxygen delivery, and renal oxygen consumption in such patients. Central hemodynamics, renal blood flow, and oxygen transport were measured in 10 patients in low cardiac output states. Measurements were made with and without intra-aortic balloon counterpulsation. Renal blood flow was measured by continuous renal vein thermodilution. Small improvements were observed in cardiac output (3.1 +/- 0.8 vs 3.5 +/- 0.8 L/min, P < .01) and pulmonary capillary wedge pressure (22 +/- 5.6 vs 19 +/- 5.3 mmHg, P < .05), but mean arterial blood pressure was unchanged (69 +/- 11 vs 69 +/- 5 mmHg, not significant). Baseline renal blood flow was reduced to approximately 37%, renal oxygen delivery to 31%, and renal oxygen consumption to 60% of normal values. No significant improvement was seen in single-kidney renal blood flow (184 +/- 108 vs 193 +/- 107 mL/min), renal oxygen delivery (28 +/- 16 vs 30 +/- 16 mL/min), or renal oxygen consumption (4.9 +/- 2.0 vs 4.7 +/- 2.5 mL/min) in response to 1:1 counterpulsation. In comparison with measurements made during short-term suspension of counterpulsation, 1:1 aortic balloon pumping failed to result in an increase in renal blood flow, oxygen delivery, or oxygen consumption from the low levels observed in these patients.     

Redistribution of collateral blood flow from necrotic to surviving myocardium following coronary occlusion in the dog

Early changes in collateral blood flow after acute coronary occlusion may be critical for survival of ischemic myocardium. We used 15-mum radioactive microspheres to study myocardial blood flow in thoracotomized dogs 10 minutes and 24 hours after occlusion of the left anterior descending coronary artery (LAD). The ischemic area was delineated by dye injected into the distal artery, and indentification of potentially ischemic samples was confirmed by a newly developed technique in which microspheres were excluded from the normally perfused LAD. Layers were separated into necrotic or normal as defined by gross inspection and confirmed by histological examination and creatine phosphokinase assay. Infarction always involved endocardial layers and extended toward the epicardium. Average myocardial blood flow in 48 necrotic samples from 16 dogs either remained low (less than 0.05 ml/min g-1) or declined, falling from 0.11 +/-0.02(SE) at 10 minutes to 0.05 +/-0.01 ml/min g-1 at 24 hours (P less than 0.001). In contrast, in the 32 normal-appearing samples which were ischemic at 10 minutes, flow increased from 0.24 +/-0.03 to 0.39 +/-0.04 ml/min g-1 (P less than 0.001). Flow in control myocardium was 1.43 +/-0.12 and 1.04 +/-0.07 ml/min g-1, respectively. Peripheral mean coronary arterial pressure increased from 26 +/- 3 to 35 +/- 3 mm Hg, largely because of enlargement of collateral vessels; collateral conductance calculated from retrograde flow in 14 dogs increased from 0.023 +/- 0.005 after occlusion to 0.051 +/- 0.009 ml/min mm Hg-1 24 hours later (P less than 0.001). Thus, coronary collateral blood flow is redistributed from necrotic endocardial layers to surviving epicardial ones. In combination with a developing collateral supply this process may be essential for sparing myocardium after coronary occlusion.     

Coronary flow analysis during autoperfusion angioplasty

BACKGROUND: Autoperfusion balloons are available for the protection of the myocardium during balloon angioplasty. The aortic pressure is the driving force that delivers blood to the distal vessel during balloon inflation. Autoperfusion balloons can achieve sufficient flow rates in vitro. The use of these devices is recommended in high-risk patients in danger of haemodynamic collapse during balloon inflation. The quantity of the distal blood flow during balloon inflation in vivo is still unknown. OBJECTIVES: To measure distal coronary perfusion using Doppler guidewires during percutaneous transluminal coronary angioplasty (PTCA) with autoperfusion balloons. METHODS: Coronary flow velocity was measured with 0.014-inch Doppler guidewires bypassing the autoperfusion balloon in eight patients undergoing elective PTCA (degree of stenosis 74 +/- 7.2%). We used balloons with diameters of 3.0 and 3.5 mm. The coronary diameter at the location of the flow measurements was obtained by quantitative angiography in two planes. Coronary blood flow was calculated as the luminal area multiplied by the average peak flow velocity of the Doppler wire divided by 2. Coronary flow velocity reserve was measured before and after angioplasty by intracoronary injection of adenosine. RESULTS: Coronary blood flow was 35 +/- 11.6 ml/min before PTCA. During average inflation times of 4.6 +/- 0.9 min, coronary blood flow was 19 +/- 3.8 ml/min (P = 0.002) after withdrawing the guidewire in the autoperfusion balloon. Five minutes after angioplasty it increased to 42 +/- 13.5 ml/min (P < 0.001). Four patients had electrocardiographic changes during balloon inflation; three patients reported chest pain. One patient required a stent because of a local dissection. To achieve satisfactory angiographic results (residual stenosis 11 +/- 8.5%), we performed 2.1 +/- 0.78 inflations on average with a cumulative inflation time of 8.8 +/- 3.35 min. Coronary flow velocity reserve increased from 1.3 +/- 0.20 to 2.2 +/- 0.22 (P < 0.001). CONCLUSIONS: Using the autoperfusion balloon we measured a coronary blood flow during angioplasty of 56 +/- 10.3% of the distal perfusion before PTCA. In high-risk patients dependent on adequate coronary perfusion, autoperfusion balloons are not able to provide sufficient distal coronary blood flow during balloon inflation. In these patients active coronary or circulatory support devices are recommended.     

Verification of a free vascularized nerve graft model in the rat with application to the peripheral nerve allograft

The effects of moderate systemic hypotension with halothane (HALO) and isoflurane (ISO) on regional myocardial function and perfusion were studied in dogs with chronic coronary artery occlusion. Vasodilator reserve in collateral-dependent (CD) myocardium was quantified in conscious animals by using a dipyridamole challenge test. Blood flow was distributed homogeneously to the normal (Nl) and CD myocardium at rest, but subendocardial perfusion increased only in the Nl area after dipyridamole. HALO and ISO were administered at doses that reduced diastolic arterial pressure to 50 mm Hg. End-tidal concentrations were 1.3 +/- 0.2 vol% for HALO (1.5 minimum alveolar anesthetic concentration) and 1.8 +/- 0.2 vol% for ISO (1.4 minimum alveolar anesthetic concentration), respectively. Global and regional hemodynamic depression were more pronounced with HALO. Systolic wall-thickening fraction decreased both in the Nl (-37%) and CD area (-27%). Myocardial blood flow to Nl and CD myocardium decreased to a comparable extent. ISO predominantly decreased systemic vascular resistance and, when compared to HALO, decreased systolic wall-thickening fraction less in both the Nl (-19%) and CD area (-18%). In addition, regional myocardial perfusion to both Nl and CD myocardium remained virtually unaltered from conscious control conditions. Despite reductions of diastolic blood pressure to 50 mm Hg, neither HALO nor ISO induced ischemic dysfunction in myocardium with diminished vasodilator reserve. Both anesthetics preserved intercoronary as well as transmural blood flow distribution. During HALO, myocardial perfusion was less both in Nl and CD myocardium due to a more pronounced metabolic depression. We conclude that moderate hypotensive doses of ISO and HALO preserve regional myocardial function of collateral-dependent myocardium in dogs with single vessel occlusion and enhanced collateral circulation.     

Sardinian alcohol-preferring rats prefer chocolate and sucrose over ethanol

The purpose of this study was to evaluate the effect of sequential external counterpulsation (SECP) on cerebral and renal blood flow. The effect of SECP on carotid and renal artery blood flow was studied in 35 and 18 patients, respectively. With a portable unit, cuffs were applied to the calves and thighs, sequentially inflated with air at the onset of diastole, and deflated at the onset of systole. Carotid and renal artery Duplex studies were performed during intermittent SECP. Flow velocity and flow velocity integral were measured at baseline and during SECP. Diastolic augmentation of carotid and renal artery flow velocity was observed in all patients. The mean carotid flow velocity integral increased by 22% from 27.7 +/- 1.8 cm to 33.1 +/- 2.3 cm (P = 0.001). The mean renal artery flow velocity integral increased by 19% from 21 +/- 1 cm to 25 +/- 1 cm (P = 0.0001). With SECP, a new diastolic Doppler flow velocity wave was observed, with an average peak carotid diastolic flow velocity of 56 +/- 4 cm/sec and an average peak renal artery diastolic flow velocity of 40 +/- 2.5 cm/sec. This diastolic wave was 75% (carotid) and 68% (renal) as high as the systolic wave during SECP. In addition, with SECP the systolic wave increased by 6% and 8% in the carotid and renal artery, respectively (P = 0.02 and 0.006, respectively). In conclusion, SECP significantly increases carotid and renal blood flow. This noninvasive, harmless treatment may be useful to support patients with decreased cerebral and renal perfusion.     

Left intraventricular balloon pump optimization during intractable cardiac arrest

This work aims to determine optimal balloon shape and volume during left intraventricular balloon pumping (IABP) in the fibrillating dog heart. A balloon volume equal to the left ventricular end-diastolic volume (LVEDV) maintained a higher systolic aortic pressure and flow (106.4 +/- 2.7 mmHg and 84.7 +/- 2.35 ml/kg/min, x +/- SEM, respectively) than a 25% smaller (97.8 +/- 3.3 mmHg, P = 0.002 and 63.7 +/- 4.1 ml/kg/min, P = 0.002, respectively) or a 25% larger balloon (87.4 +/- 2.3 mmHg, P = 0.002 and 70.9 +/- 3.4 ml/kg/min, P = 0.002, respectively). Among 5 different balloon shapes tested, a pear-shaped balloon inflated from the apex to the base of the left ventricle induced the highest (P varying from 0.042 to 0.01, compared to the remaining balloon shapes) systolic aortic pressure and flow (104.6 +/- 4.5 mmHg and 77.9 +/- 1.7 mg/kg/min, respectively). In conclusion, a pear shaped balloon, inflated to a volume equal to the LVEDV, from the apex to the base of the left ventricle, induced an optimal hemodynamic effect during LVBP.     

Allyl sulfides from garlic suppress the in vitro proliferation of human A549 lung tumor cells

This study was designed to evaluate the alterations in doppler derived coronary blood flow velocities and flow reserve following rotational ablation. Changes in doppler derived coronary blood flow velocity variables have been valuable in assessing the physiological outcome following coronary balloon angioplasty. Rotational ablation's mechanism of plaque removal could alter distal vascular bed characteristics, and, as a result, intracoronary blood flow velocities and the coronary flow reserve. A 12-MHz doppler guidewire recorded intracoronary phasic velocities and coronary flow reserve (as assessed by the hyperemic response to adenosine [12-18 mcg intracoronary]) in 28 patients, before and after rotational ablation of 30 lesions. Adjunctive balloon angioplasty was performed in 27 of 28 patients (96%). Rotational ablation and adjunctive balloon angioplasty successfully reduced the lesion diameter (87 +/- 9% to 14 +/- 11%; P < 0.001). A significant increase in the mean distal average peak velocity (25 +/- 13 cm/sec, before; 47 +/- 22 cm/sec, after; P < 0.001), and decrease in the proximal to distal average peak velocity ratio, (2.1 +/- 1.3; to 1.2 +/- 0.4; P = 0.002) was recorded. The mean distal diastolic to systolic velocity ratio (before, 1.4 +/- 0.7; after, 1.6 +/- 0.8; P = 0.44) and the coronary flow reserve (before, 1.6 +/- 0.6; after, 1.5 +/- 0.5; P = 0.34) did not increase despite increases in distal velocities, following successful intervention. Doppler derived distal coronary blood flow velocities increased following rotational ablation and adjunctive balloon angioplasty, with resolution of transstenotic velocity gradient. Changes in distal phasic velocity pattern and coronary flow reserve, immediately after the intervention, were not useful in the assessment of the functional outcome and may be related to abnormalities in distal vascular bed vasoreactivity produced by rotational ablation.     

Coronary steal: its role in detrimental effect of isoproterenol after acute coronary occlusion in dogs

Using epicardial electrograms others have established that infusion of isoproterenol increases myocardial injury after acute coronary occlusion. To define the contribution of alterations in collateral blood flow to this increased ischemia, isoproterenol was administered to 10 dogs. After pretreatment with practolol in doses that successfully block inotropic but not vascular effects of beta adrenergic stimulants, intracoronary isoproterenol continued to enhance the magnitude of S-T segment elevation in ischemic areas. Thus, vasodilation induced by isoproterenol appears to divert flow from the ischemic area. To test this hypothesis, intracoronary adenosine was given to cause coronary vasodilation without enhancing inotropy. S-T segment elevation at ischemic and adjacent sites was significantly increased. Neither agent had systemic effects, but each increased coronary blood flow while concomitantly decreasing collateral flow as evidenced by a reduction in retrograde coronary flow and peripheral coronary pressure. In addition, adenosine significantly diminished the rate of xenon-133 clearance from the ischemic myocardium. Thus, isoproterenol, in addition to its positive inotropic effect, increases myocardial injury by its vascular action. Collateral blood flow to acutely ischemic myocardium is diminished by the production of a coronary steal. Intravenously administered isoproterenol additionally diminishes collateral flow by decreasing coronary perfusion pressure. It is postulated that any agent that causes either a primary or secondary coronary vasodilation may cause a coronary steal and subsequently enhance myocardial injury.     

Acadesine increases blood flow in the collateralized heart during exercise

Acadesine, an adenosine-regulating agent, has been shown to increase coronary flow and exert cardioprotective effects in acutely ischemic myocardium, but a beneficial effect on coronary collateral flow during exercise has not been demonstrated. We examined the effect of acadesine, 100 micromol/min, i.v., on myocardial blood flow during treadmill exercise in six normal dogs and seven dogs with moderately well-developed coronary collateral vessels. Collateral vessel growth was produced with 2-min intermittent occlusions of the left circumflex coronary artery followed by permanent occlusion. During resting conditions, myocardial blood flow in the collateral zone was not significantly less than in the normal zone, but during exercise, blood flow increased by only 79 +/- 21% (from 0.98 +/- 0.29 ml/min/g to 1.64 +/- 0.19 ml/min/g; p < 0.05) in the collateral zone as compared with 118 +/- 32% (from 1.09 +/- 0.28 ml/min/g to 2.14 +/- 0.2 ml/min/g; p < 0.01) in the normal zone. During exercise, acadesine further increased mean blood flow in the collateral-dependent region by 24 +/- 5% (to 2.04 +/- 0.26 ml/min/g; p < 0.05) with no change in the transmural distribution of perfusion. The increase in collateral zone blood flow in response to acadesine resulted from a decrease in both transcollateral resistance from 25.1 +/- 2.7 mm Hg/min/g/ml to 18.8 +/- 8 mm Hg/min/g/ml (p < 0.05) and small-vessel resistance in the collateral-dependent myocardium from 45.3 +/- 6.6 mm Hg/min/g/ml to 36.4 +/- 5.8 mm Hg/min/g/ml (p < 0.05). Acadesine also significantly increased normal-zone flow in the collateralized dogs (to 2.62 +/- 0.33 ml/min/g; p < 0.05). In contrast, acadesine had no effect on coronary blood flow in normal dogs. In dogs with moderately well-developed collateral vessels, acadesine increased blood flow in both the collateral-dependent and normal myocardial zones during exercise. In contrast, acadesine did not increase blood flow in normal dogs. These findings suggest that adenosine metabolism is altered not only in the collateral-dependent region but also in the normal region of hearts with a coronary artery occlusion.     

Perfusion of ischemic myocardium during anesthesia with sevoflurane

BACKGROUND: Sevoflurane produces direct vasodilation of coronary arteries in vitro and decreases coronary vascular resistance in vivo, pharmacologic properties that may contribute to the development of "coronary steal." This investigation examined the effects of sevoflurane on the distribution of regional myocardial perfusion in chronically instrumented dogs with steal-prone coronary artery anatomy. METHODS: Dogs were chronically instrumented for measurement of aortic and left ventricular pressure, diastolic coronary blood flow velocity and subendocardial segment length. After recovery from surgery, dogs underwent repetitive, brief, left anterior descending coronary artery (LAD) occlusions via an implanted hydraulic vascular occluder to enhance collateral development. A progressive left circumflex coronary artery (LCCA) stenosis was also obtained using an ameroid constrictor. After development of LCCA stenosis, the LAD was totally occluded to produce a model of multivessel coronary artery disease. Systemic hemodynamics, regional contractile function and myocardial perfusion measured with radioactive microspheres were assessed in the conscious state and during sevoflurane anesthesia at 1.0 and 1.5 MAC with and without restoration of arterial blood pressure and heart rate to conscious levels. RESULTS: Total LAD occlusion with simultaneous LCCA stenosis increased heart rate, mean arterial pressure, left ventricular systolic and end-diastolic pressures, end-diastolic segment length, and rate-pressure product in conscious dogs. Subsequent administration of sevoflurane caused dose-related decreases in arterial pressure, left ventricular systolic pressure, double product, and peak rate of increase of left ventricular pressure at 50 mmHg. Perfusion of normal myocardium was unchanged during sevoflurane anesthesia. In contrast, sevoflurane caused dose-dependent decreases in blood flow to myocardium supplied by the stenotic LCCA, which returned to control levels after restoration of heart rate and arterial pressure. No reduction in collaterally derived blood flow to the occluded region was produced by 1.0 or 1.5 MAC sevoflurane. No redistribution of blood flow away from the occluded LAD region to normal or stenotic myocardium occurred during sevoflurane anesthesia. In fact, increases in the ratio of blood flow between occluded and normal zones or occluded and stenotic zones were observed in the subepicardium during 1.5 MAC sevoflurane with maintenance of the heart rate and arterial pressure at conscious levels. CONCLUSIONS: The results demonstrate that sevoflurane does not reduce or abnormally redistribute myocardial blood flow derived from coronary collateral vessels in a chronically instrumented canine model of multivessel coronary artery obstruction.     

The effect of hemodilution with stroma-free hemoglobin and dextran on collateral perfusion of ischemic myocardium in the dog

The effect of hemodilution with stroma-free hemoglobin (SFH) solution was assessed on the collateral perfusion of acutely ischemic myocardium in anesthetized dogs. A similar protocol was used in three groups: one hour following occlusion of the LAD coronary artery, a rapid exchange-transfusion was performed and the changes were followed for the subsequent two hours. Group I was hemodiluted with SFH, in Group II whole blood was reinfused, and Group III was hemodiluted with dextran 70. Following the exchange-transfusions, blood flow to the ischemic zone (15 +/- 3 micrometer microspheres) increased in all groups, but only marginally so in Group II (23 +/- 17%). The greatest increments were seen in the SFH-hemodiluted group (Group I) in which endocardial flow increased by 83 +/- 29% (p less than .05) and epicardial flow increased by 45 +/- 21%; these resulted in the greatest improvements in oxygen delivery. Significant increments in blood flow were seen in Group III, as well, but oxygen delivery was less adequate. Group I also exhibited the lowest output of CPK from the heart and was the only one in which indices of left ventricular performance (dP/dt and EDP) were returned to the pre-occlusion level. these findings suggest the possibility that reduction of blood viscosity by dilution with SFH improves collateral perfusion of the ischemic myocardium.     

Effects of sotalol and vagal stimulation on ischemic myocardial blood flow distribution in the canine heart

The purpose of the present study was to compare the effect of equivalent decreases in heart rate produced by sotalol and bilateral vagal stimulation on regional myocardial blood flow and coronary perfusion pressure distal to a severe stenosis of the left circumflex coronary artery in anesthetized dogs. Tissue blood flow was measured with radioactive microspheres (15 mu). Vagal stimulation or beta adrenergic blockade produced by sotalol (1.0 mg/kg i.v.) reduced heart rate approximately 35 beats/min. This decrease in rate was accompanied by nearly equivalent increases (P less than 0.05) in diastolic perfusion time and subendocardial blood flow and in the ischemic region. Both interventions also significantly increased the oxygen supply-demand balance (distal diastolic pressure time index divided by the tension time index) in the ischemic region. These values returned to control after cessation of vagal stimulation or during atrial pacing to predrug heart rate. Coronary perfusion pressure distal to the stenosis increased significantly only in the sotalol-treated group. These results suggest that a decrease in heart rate and increase in diastolic perfusion time are important factors in the favorable redistribution of ischemic myocardial blood flow and increase in the oxygen supply-demand balance observed after beta adrenergic blockade with sotalol or after vagal stimulation. Whether these beneficial actions are solely due to the prolonged diastolic perfusion period or to reduced oxygen demand and a return to autoregulation in the ischemic area cannot be determined with certainty.     

Inhibition of angiotensin-converting enzyme increases the nitric oxide levels in canine ischemic myocardium

Since angiotensin-converting enzyme (ACE) produces angiotensin II in the heart, ACE inhibitors may prevent coronary vasoconstriction and increase coronary blood flow. On the other hand, since ACE inhibitors also inhibit kininase II which results in reduced degradation of bradykinin, ACE inhibitors may increase cardiac nitric oxide (NO) levels via stimulation of bradykinin receptors. This study was undertaken to test whether ACE inhibitors increase the cardiac NO levels and coronary blood flow in the ischemic myocardium. In 34 open-chest dogs, the left anterior descending coronary artery was perfused through an extracorporeal bypass tube from the left carotid artery. When either imidaprilat or cilazaprilat of 3 microg/kg/min was infused into the bypass tube for 10 min after reduction of coronary blood flow due to partial occlusion of the bypass tube, coronary blood flow increased from 31 +/- 1 to either 45 +/- 5 or 43 +/- 4 ml/100 g/min despite no changes in coronary perfusion pressure (43 +/- 2 mmHg). During an infusion of either imidaprilat or cilazaprilat, bradykinin and the end-products of NO (nitrate + nitrite) concentrations of coronary venous blood were markedly increased, which were attenuated by either HOE-140 (an inhibitor of bradykinin receptors) or by N(omega)-nitro-L-arginine methyl ester (an inhibitor of NO synthase). We also observed increases in cardiac bradykinin and NO levels due to either imidaprilat or cilazaprilat in the low constant coronary blood flow condition. It is concluded that ACE inhibitors can increase cardiac NO levels via the accumulation of bradykinin in the ischemic myocardium.     

High stroke volume para-aortic counterpulsation device versus centrifugal pump in cardiogenic shock: experimental study

During the last decades a number of left ventricular assist devices has been used especially for patients resistant to pharmacologic treatment and to intraaortic balloon pump (IABP) support for left ventricular failure. A high stroke volume para-aortic counterpulsation device (PACD) has been developed utilizing the principle of the diastolic counterpulsation technique. In this study the hemodynamic effects of the valveless PACD were compared to those of the centrifugal blood pump (CBP) in nine dogs in acute experimental cardiogenic shock. Hemodynamic measurements were obtained at baseline with both devices off, PACD on and CBP off, or PACD off and CBP on. There was no difference in mean aortic pressure between PACD on (60.0 +/- 11.5 mmHg) and CBP on (69.0 +/- 26.8 mmHg). Similarly, there was no difference in left ventricular end-diastolic pressure with the PACD on (11.9 +/- 5.4 mmHg) versus the CBP on (9.9 +/- 5.2 mmHg) or the cardiac index with the PACD on (84 +/- 36 ml/kg/min) versus the CBP on (77 +/- 36 ml/kg/min). However, the left ventricular systolic pressure (55.0 +/- 19.0 with PACD versus 73.0 +/- 26.0 with CBP,p < 0.001), the tension time index (712 +/- 381 versus 1333 +/- 694,p < 0.01), and the double product (5629 +/- 2574 versus 7440 +/- 3294,p < 0.01) were significantly lower during assistance with the PACD than with the CBP. It was concluded that PACD is at least as effective as CBP for restoring hemodynamic status during acute experimental cardiogenic shock. Moreover, the PACD unloads the left ventricle more effectively than CBP, making it suitable for left ventricular mechanical support in cases with reversible myocardial damage.     

Left ventricular diastolic function in young men with high normal blood pressure

OBJECTIVE: Abnormalities in left ventricular (LV) diastolic filling have been reported in hypertensive patients. This study was designed to compare LV diastolic filling between individuals with high normal blood pressure (HNBP) and optimal blood pressure (OBP). SUBJECTS AND DESIGN: From a survey of 219 young male individuals (age 21 +/- 0.1 years), two groups were selected according to their BP (group A: systolic BP [SBP] 120 mmHg and diastolic BP [DBP] 80 mmHg, n = 23 and group B: SBP 130 to 139 mmHg and/or DBP 85 to 89 mmHg, n = 21). Subjects habits, anthropometric characteristics, LV structure and systolic and diastolic function were compared. RESULTS: No differences were detected between the two groups in habits, systolic function or early diastole. LV mass index (LVMI) was higher in group B (103.6 +/- 4.58 g/m2 versus 90.49 +/- 3.27 g/m2 in group A, P < 0.05), though the values were not high enough to indicate LV hypertrophy. The pattern of LV late filling was different between the two groups. The peak late diastolic flow velocity (A) was 0.45 +/- 0.02 m/s in group B and 0.52 +/- 0.03 m/s in group A (P < 0.05). The early peak velocity (E):A ratio was 1.82 +/- 0.08 in group A and 1.59 +/- 0.08 in group B (P < 0.05). The early filling fraction also demonstrated a significant shift to more prominent late diastolic filling in group B (0.68 +/- 0.01% versus 0.73 +/- 0.01% in group A, P < 0.05). This pattern in LV filling did not correlate to inheritance, age, sex, heart rate, habits or body mass index. CONCLUSIONS: This shift in filling pattern to a late flow in young men with HNBP seemed to be an early indicator of an increased dependence of LV filling on atrial contraction and may reflect an impairment in LV relaxation.     

The concept of "direct mechanical ventricular assistance" in the treatment of left-ventricular failure. Part 2. Results of the new intrathoracic implantable multi-chamber pump system (IMPS) in an animal study

An assist device was developed which is able to support the pumping function of the heart by direct application of pressure to the left ventricle. The goal of this animal study in pigs was to determine whether it is possible to maintain sufficient blood circulation with the aid of the new system when the heart is fibrillating or its capacity has been greatly reduced. Following sternotomy complete invasive monitoring was installed. The intrathoracic implantable mechanical multi-chamber pump system (IMPS) was placed around the left ventricle. By means of the beta-blocker carazolol, systolic left-ventricular pressure (LVPsys), cardiac output, heart rate, and left-ventricular dp/dtmax (LVdp/dtmax) were gradually lowered and the pump system was tested intermittently. Then the heart was fibrillated and the system was tested again. When cardiac output, LVdp/dtmax, and systolic blood pressure were reduced by approximately 50% IMPS was able to increase LVPsys by 83% (IMPS) on: 96 +/- 9 mmHg vs. IMPS off: 63 +/- 6 mmHg), and the blood pressure in the carotid artery by 86% (IMPS on: 95/40 +/-15 mmHg vs. IMPS off: 69/38 +/- 9 mmHg). The mean cardiac output was 64% (IMPS on: 4.3 L/min vs. IMPS off: 3.9L/min); in most cases a great variability could be observed depending on the preload, the heart rate, and the mode of pressure application. When the heart was fibrillating, IMPS was able to maintain adequate circulatory conditions with LVPsys = 88%, blood pressure in the carotid artery = 85%, and LVdp/dtmax = 57% of the control values measured before fibrillation and beta-blockade. The system presented here is able to support the impaired left ventricle and to replace its pumping function. The advantages of the system are its efficiency and the lack of contact of the circulating blood with foreign surfaces. Whether the system is suited for bridging and recovery support shall be clarified in further studies.     

Long-term antihypertensive therapy with isradipine. Improvement of coronary flow reserve in patients with arterial hypertension and microvascular angina

Antihypertensive Long-term Therapy with Isradipine/Improvement of coronary flow reserve in patients with arterial and microvascular angina In patients with arterial hypertension coronary flow reserve is often impaired due to left ventricular (LV) hypertrophy and alterations of the coronary microcirculation. Experimental and clinical studies have shown that calcium channel blockers can induce regression of myocardial hypertrophy. Objective of the present study was to see whether chronic antihypertensive treatment with calcium channel blockers can improve the diminished coronary reserve in patients with arterial hypertension and microvascular angina pectoris. Fifteen hypertensive patients with microvascular angina (61 +/- 7 years, normal coronary angiogram, mild LV-hypertrophy) were treated with isradipine (CAS 75695-93-1) (5.3 +/- 0.9 mg/d) for 12 +/- 2 months. Before and after therapy (after a washout period of 1 week) coronary flow was quantitatively measured by the gas chromatographic Argon method. Coronary reserve was calculated as the quotient of coronary resistance under baseline conditions and after dipyridamole (0.5 mg/kg i.v.). Under isradipine therapy systolic blood pressure was lowered from 165 +/- 20 to 140 +/- 13 mmHg (p < 0.01) and diastolic blood pressure from 98 +/- 8 to 88 +/- 6 mmHg (p < 0.01). The LV muscle mass index decreased by 10% from 154 +/- 33 to 139 +/- 28 g/m2 (p < 0.05). Baseline coronary blood flow (81 +/- 13 versus 83 +/- 16 ml/min x 100 g, n.s.) was identical before and after therapy. There were also no differences in coronary perfusion pressure, heart rate, myocardial oxygen consumption and arterio-coronary venous oxygen difference before and after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular diastolic chamber stiffness and intramyocardial coronary capacitance in isolated dog hearts

BACKGROUND: Because the myocardium is perfused primarily during diastole, changes in diastolic properties of the left ventricle (LV) should influence the intramyocardial circulation. METHODS AND RESULTS: We examined the influence of LV diastolic properties on the magnitude and localization of intramyocardial coronary capacitance by analyzing the coronary pressure-venous flow relation in isolated, isovolumic dog heart preparations. After sudden occlusion of the left coronary artery during a long diastole, we measured precapacitance and postcapacitance resistances (RPRE and RPOST) and calculated intramyocardial coronary capacitance (CIM) from RPOST and the time constant of the coronary venous flow decay. Using this method, we characterized the effects of coronary vasodilation, LV diastolic volume, and LV diastolic chamber stiffness on the coronary circulation. The magnitude of CIM increased from 0.09 +/- 0.01 to 0.24 +/- 0.20 mL.mm Hg-1 x 100 g-1 (P < .01) after adenosine-induced vasodilation, whereas both RPOST and RPRE decreased significantly. The ratio of RPOST to RPRE+RPOST decreased from 0.35 +/- 0.02 to 0.23 +/- 0.02 (P < .01), suggesting redistribution of CIM to the distal portion of the coronary vascular tree. An increase in LV volume and wall stress was imposed to increase LV diastolic pressure from 2 +/- 0.1 to 25 +/- 1 mm Hg: this increased RPOST significantly but not RPRE and decreased the magnitude of CIM. The resistance ratio did not change significantly. Increased LV diastolic chamber stiffness induced by hypoxic perfusion (isovolumic LV diastolic pressure increased from 11 +/- 1 to 28 +/- 1 mm Hg) raised RPOST and decreased the magnitude of CIM from 0.32 +/- 0.12 to 0.17 +/- 0.04 mL.mm Hg-1 x 100 g-1 (P < .05). The resistance ratio increased significantly from 0.21 +/- 0.05 to 0.33 +/- 0.05 with increased LV diastolic chamber stiffness. Adjustment of LV diastolic volume to lower diastolic pressure to 10 +/- 1 mm Hg did not alter these changes significantly, suggesting that an intrinsic increase in myocardial stiffness played a major role in these changes. CONCLUSIONS: Extravascular compression by raised LV diastolic volume and/or increased LV diastolic chamber stiffness acted mainly on coronary vessels that determine intramyocardial capacitance and postcapacitance resistance.     

Phasic changes in human right coronary blood flow before and after repair of aortic insufficiency

We have shown previously that acute aortic insufficiency in chronically instrumented dogs reverses the normally high ratio of diastolic to systolic coronary blood flow. Phasic blood flow in the dominant right coronary artery was measured directly with an electromagnetic flow meter during surgery in eight patients with severe aortic insufficiency before and after relacement of the aortic valve. Before the insufficiency was eliminated, right coronary flow average 116 +/- 37 ml./minute and the diastolic to systolic flow ratio was 0.88 +/- 17. Mean arterial blood pressure averaged 106 +/- 17 mm. Hg, heart rate 84 +/- 19 beats/minute, and mean diastolic pressure averaged 67 +/- 10 mm. Hg. After the aortic valve was replaced with an average heart rate of 90 +/- 15 and mean blood pressure of 103 +/- 13 mm. Hg, the average right coronary blood flow increased to 180 +/- 40 ml./minute with a D/S ratio of 2.18 +/- 0.8. In all cases the right coronary blood flow increased after the aortic insufficiency was eliminated surgically. Right coronary flow probably increased because of the improved diastolic perfusion pressure and the change from predominantly systolic to diastolic coronary flow.