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Heparin-induced thrombocytopenia (HIT) is the most common drug-related thrombocytopenia. Thromboembolic complications occur in approximately 50% of patients with HIT and result in limb amputation and death in up to 20% and 30% respectively. Because patients with a history of HIT may require future intravenous anticoagulation but have a high-risk of thromboembolism if re-challenged with heparin, alternative therapies are necessary when further anticoagulation is indicated. The use of direct thrombin inhibitors in HIT patients who also require thrombolytic therapy offers unique challenges to anticoagulant monitoring and safety. We present a case of progressive ileofemoral deep venous thrombosis in a patient with a history of HIT in order to review the combined use of hirudin and thrombolysis in this setting.

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Signal averaging can be used to assess changes in myocardial activation under a variety of physiological conditions including stress. This study prospectively evaluated patients who underwent rest and exercise recording of signal-averaged electrocardiograms. The 163 patients were divided into three groups based on thallium results: normal (group I), reperfusion (group II), and fixed defect (group III). Patients in group I showed shortening of the high frequency duration (P = 0.02) and the duration of the low amplitude signal (P = 0.024) after exercise. In these patients the terminal root mean square amplitude (RMSA) also increased significantly (P = 0.005). However, patients who were in either group II or group III showed little change in signal averaging measurements after exercise. The amplitude of the QRS in V5 and the RMSA of the total QRS also increased in all groups following exercise, with a lesser increase in the patients with reperfusion by thallium imaging (group II). There was no change among groups in the incidence of ventricular late potentials with exercise. This suggests that patients with ischemia or infarction may not have the same response to an increase in sympathetic tone with exercise as patients without abnormalities of cardiac perfusion. The clinical implications of these findings may include demonstration that an area of slow conduction exists in these latter two groups of patients.

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OBJECTIVE: The aim of the study was to assess the contraction of myocardium stunned by repetitive brief coronary occlusions by examining the response to alterations in loading and inotropy of systolic contraction on isovolumetric and ejection phase shortening. METHODS: Fourteen open chest anaesthetised dogs were used for the studies. After destruction of the sinus node, the heart was atrially paced and atrial extrasystoles were introduced followed by a short (400 ms) or long (700 ms) postextrasystole. The left anterior descending coronary artery was occluded for 5 min and reperfused for 10 min a total of eight times to produce stunned myocardium, followed by a final 60 min of reflow. Regional function was assessed with segment length sonomicrometers. RESULTS: With successive periods of occlusion there was an increase in the end diastolic segment length and a progressive decrease in total percent systolic shortening (baseline 22.3%, 1st reflow 14.5%, 8th reflow 7.9%) with some recovery after 60 min of reflow (12.0%). This was predominantly due to the development of bulging during isovolumetric systole (4.5%, -4.9%, and -8.3%, respectively) which diminished during 60 min recovery to -3.1%. Ejection shortening was relatively constant (17.8%, 19.4%, 16.3%, and 15.1%, respectively). Postextrasystolic potentiation resulted in an increased in total percent systolic shortening, but not to the baseline value, as slight isovolumetric bulging persisted. Similar changes were seen with the short and long postextrasystoles although the latter had a greater increase in ejection shortening. CONCLUSIONS: The decrease in function after repetitive occlusion and reflow is predominantly due to bulging during isovolumetric systole which persists after postextrasystolic potentiation in our model of stunned myocardium.

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The purpose of this study was to determine if mannitol stimulates atrial natriuretic peptide (ANP) release in humans and to examine potential mechanisms for this effect. Twenty patients requiring cardiac catheterization were randomized to receive either mannitol (15-g bolus followed by 15% infusion mixed in 75 mmol/L saline at 100 mL/h for 1 hour) or an equal volume of 75 mmol/L saline, intravenously (IV). All measurements were made at three time points: at baseline, at 10 minutes (after the bolus but before radiocontrast administration), and at 60 minutes (after completion of the study). Baseline plasma ANP (PANP) measurements (mean +/- SE) were similar in both groups (saline, 73 +/- 38 pg/mL; mannitol, 62 +/- 11 pg/mL). PANP increased significantly over time for the set of all patients (analysis of variance [ANOVA], P less than 0.05); however, at 10 minutes PANP increased significantly only in the group receiving mannitol (saline, 76 +/- 43 pg/mL; mannitol, 100 +/- 29 pg/mL) (P less than 0.04). Serum osmolality (SOSM), over time for the set of all patients (ANOVA, P less than 0.04). At 10 minutes there were significant increases only in the group receiving mannitol, and after radiocontrast, there were significant increases in both groups for all parameters. Regression analysis demonstrated a significant correlation between the change in PANP and the change in SOSM (P less than 0.04, r = 0.33). In conclusion, intravascular infusion of mannitol or radiocontrast increased PANP levels. The mechanism may be multifactorial, with a potential role for an increase in SOSM and/or PADH.

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Because the extent of myocardial bulging after acute coronary occlusion is primarily dependent on wall tension, this study examined whether the decrease in systolic bulging with postextrasystolic potentiation was due to contractile reserve or to changes in loading conditions. Seven dogs were atrially paced at 100 beats/min after the sinus node was crushed and atrial extrasystoles were generated. The left ventricular minor axis diameter and segment lengths in the ischemic and nonischemic zones were measured with sonomicrometers. Wall tension was estimated using Laplace's law, and regional tension-length loops were determined. By 5 min after the left anterior descending coronary artery was occluded, there was regional bulging. Postextrasystolic potentiation diminished the extent of bulging by increasing both isovolumic and ejection percent systolic shortening (isovolumic -9.1 +/- 2.0% to -5.9 +/- 1.7%, p less than 0.008; ejection 2.2 +/- 0.7% to 4.3 +/- 2.0%, p less than 0.008). The tension-length loops after coronary occlusion showed an exponential upstroke and almost superimposed downstroke consistent with passive movement. The loops were unchanged by postextrasystolic potentiation. Wall tension data showed that bulging was reduced because of a shift down the tension-length curve as end-systolic wall tension was reduced by augmented nonischemic contraction. Similar results were seen at 60 min of coronary occlusion. This study demonstrates that the decrease in bulging seen with postextrasystolic potentiation is due to changes in loading conditions and not to contractile reserve.

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Regional function assessed by ventriculography may be influenced by the hemodynamic effects of rapidly injecting ionic contrast medium. The importance of this after acute coronary occlusion was examined in eight open-chest, anesthetized dogs. The left anterior descending artery was ligated while sonomicrometric segment lengths in the ischemic (IZ) and nonischemic zones (NZ) were measured. Sodium methylglucamine diatrizoate (Renografin-76, 1 ml/kg) was rapidly injected over 3 seconds. Fifteen minutes later, the left ventricular end-diastolic pressure (LVEDP) was rapidly increased to the level reached during injection. Injecting the contrast increased the LVEDP (7.3 +/- 2.5 to 20.1 +/- 2.9 mm Hg, p less than 0.0001) to the same extent as raising LVEDP (7.6 +/- 2.5 to 10.1 +/- 2.9 mm Hg, p less than 0.0001). Injecting the contrast medium increased IZ total percent systolic shortening (% delta L) (-3.90 +/- 4.43% to -2.68 +/- 4.77%, p less than 0.001) by decreasing isovolumic bulging (-6.68 +/- 4.09% to -5.49 +/- 3.33%, p less than 0.001) with little change in ejection % delta L. NZ total % delta L tended to increase (19.03 +/- 6.53% to 19.94 +/- 6.27%, p = 0.015) because of augmented ejection % delta L (13.12 +/- 2.51% to 13.71 +/- 3.10%, p = 0.017) by the Starling mechanism. Increasing the LVEDP had the same effect on IZ and NZ regional shortening as injecting contrast. Thus regional shortening after acute coronary occlusion is affected by the changes in loading conditions with ionic contrast ventriculography.(ABSTRACT TRUNCATED AT 250 WORDS)

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Numerous controlled studies have shown that nitrates, beta blockers, and calcium antagonists are effective in the treatment of stable angina pectoris. The pharmacokinetics, pharmacodynamics, and hemodynamic effects of these agents are different, and thus combination therapy offers additive improvement and also counterbalancing of the undesirable side effects of each drug. The choice of therapy depends on the severity of symptoms, associated diseases, compliance, side effects, and status of left ventricular function. The main mechanism of improvement is a decrease in myocardial oxygen consumption, though an increase in coronary blood flow is another potential reason for the use of calcium blockers. This review considers the properties of these drugs, their mechanism of action, and the results of randomized studies.

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We studied how left ventricular loading conditions and the size of the ischemic zone affect regional segmental shortening (% delta L) in ischemic (IZ) and remote nonischemic zones (NZ) after acute coronary occlusion. Distal and proximal portions of the left anterior descending artery (group I, 10 dogs) or the left circumflex artery (group II, 10 dogs) were occluded in two stages. Segment length sonomicrometers were placed in the distal and proximal IZ and in the distal and proximal NZ. % delta L was divided into isovolumic and ejection phases. Left ventricular end-diastolic pressure (LVEDP) was decreased 3 +/- 1 mmHg by blood withdrawal and then increased 6 +/- 2 mmHg by blood transfusion before and after distal and proximal coronary occlusions. LVEDP was brought back to its initial value before distal and proximal coronary occlusions. Regional blood flow and total blood flow deficit were measured with microspheres. Similar results were obtained in group I and II experiments. After coronary occlusion, the IZ showed systolic bulging occurring primarily in isovolumic systole. In the NZ, total and isovolumic % delta L increased from control, whereas ejection % delta L did not change. As LVEDP was raised, IZ isovolumic bulging decreased and ejection % delta L was unchanged, whereas NZ isovolumic % delta L decreased and ejection % delta L increased. Thus IZ bulging and NZ isovolumic % delta L changed in opposite directions when load was varied. The larger IZ after proximal coronary occlusion tended to increase the amount of NZ isovolumic % delta L. In conclusion, at low LVEDP NZ augmentation is predominantly caused by an increase in isovolumic % delta L, whereas if LVEDP is increased it is because of an increase in ejection % delta L. In addition, in open-chest animals augmented contraction in the NZ may be related to the size of the IZ.

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In order to optimize overall cardiac image quality on MR images experienced observers were asked to rank and rate MR images of the heart. The effect of phase-encoding direction and use of cardiac triggering with and without respiratory gating was examined in three orthogonal imaging planes. Results indicate that use of both respiratory and cardiac gating yields the best images. Adequate images of the heart can be obtained without respiratory gating. The quality of images of the heart can be optimized by proper selection of the direction of the phase-encoding gradient. These are improved by using horizontal phase encoding in the sagittal plane and vertical phase encoding in transverse and coronal planes.

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The hypothesis that there is a lateral border zone with function intermediate to adjacent ischaemic and non-ischaemic tissue was tested in 10 open chest anaesthetised dogs. Four pairs of segment length crystals were placed in parallel so as to span the ischaemic and non-ischaemic zones. Graded occlusion was produced with a screw clamp applied to a carotid to left anterior descending artery cannulation system. Contractile reserve was assessed using postextrasystolic potentiation. A balloon perfusion labelling system was used to label negatively the potentially ischaemic zone and quantify the admixture of ischaemic and non-ischaemic tissue in the lateral border zone, defined by the fraction of normal zone tissue. When the 40 crystal pairs from the 10 dogs were grouped according to fraction of normal zone tissue (FNZT), 13 were in the central ischaemic zone (FNZT less than 0.1), seven were in the border ischaemic zone (FNZT 0.1-0.5), five were in the border non-ischaemic zone (FNZT 0.5-1.0), and 15 were in the non-ischaemic zone (FNZT 1.0). When the lateral border zone is predominantly non-ischaemic tissue, the tissue behaves as though it is non-ischaemic. Segmental shortening before and after postextrasystolic potentiation in the border non-ischaemic zone and non-ischaemic zone did not change with ischaemia. When tissue in the lateral border zone is predominantly ischaemic, it behaves as though it is ischaemic. Segmental shortening decreased in parallel with progressive ischaemia in the border ischaemic zone and ischaemic zone. At total occlusion, segmental shortening in the border ischaemic zone was -2.3(5.9%) and in the ischaemic zone -3.5(3.6)% (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

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Although coronary artery disease (CAD) may be asymptomatic, it is the most common cause of death in elderly patients in the U.S. This study examined the prognosis of 449 patients with a mean age of 65 years using exercise thallium-201 imaging. At a follow-up of 25 months, 45 patients underwent coronary artery revascularization, 8 died of cardiac causes and 10 had nonfatal acute myocardial infarctions (AMIs). Thus the total of patients with "hard" events was 18. The events included 12 of 276 patients with atypical or non-anginal symptoms versus 6 of 128 with typical angina (p = not significant); 7 of 51 patients (14%) with Q-wave AMI versus 11 of 353 (3%) without Q-wave AMI (p less than 0.001); 1 of 183 patients (1%) with normal versus 17 of 221 (8%) with abnormal exercise thallium-201 images (p less than 0.002); 10 of 76 patients (13%) with multi vessel thallium-201 abnormality vs 8 of 328 (2%) with no or 1-vessel thallium-201 abnormality (p less than 0.001) and 10 of 96 patients (10%) with greater than or equal to 3 abnormal segments by thallium-201 imaging (total segments = 9) versus 8 of 308 patients with no or less than 3 abnormal segments (p less than 0.001). The number of segments with thallium-201 defects was 1 +/- 2 patients without and 3 +/- 2 in patients with hard events (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

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Dipyridamole cardiac imaging is a useful alternative technique to exercise stress testing in the evaluation of patients with ischemic heart disease. Intravenous dipyridamole is still in the investigational phase, while oral dipyridamole is widely available. The hemodynamic effects of dipyridamole include an increase in coronary blood flow (due to coronary vasodilation) which is in excess of the increase in myocardial oxygen consumption and cardiac output. The disparity in the increase in coronary blood flow relative to the cardiac output results in an increase in myocardial thallium activity and an increase in the myocardial/background activity ratio. The quality of the thallium images is better or similar to that of exercise thallium images. The optimal dose of intravenous dipyridamole is 0.56 mg/kg, and of the oral dose it is 300 to 400 mg, although higher doses may be necessary in some patients. Analysis of the thallium images has been to a large extent based on visual inspection of the planar images. Delayed images are helpful to establish the nature of the perfusion abnormalities (transient or fixed). The process of redistribution is based on disparate rates of washout from the normal and abnormal zones. The sensitivity and specificity of dipyridamole thallium imaging, whether intravenous or oral, have been shown in a number of studies to be quite adequate and comparable to that achieved during exercise thallium imaging. Dipyridamole two-dimensional echocardiography has also been used in the detection of coronary artery disease; transient (new or worsening of preexisting) wall motion abnormalities have been found to be a specific marker of coronary artery disease. Transmural as well as regional coronary steal phenomena have been postulated as the mechanism for dipyridamole-induced regional wall motion abnormalities. Compared to exercise two-dimensional echocardiography, dipyridamole echocardiography provides high-quality studies and in higher proportions of patients. The results of dipyridamole thallium imaging have also been extremely important in identifying high-risk patients after acute myocardial infarction or patients with peripheral vascular disease undergoing elective vascular surgery; the presence of a dipyridamole-induced perfusion abnormality identifies patients at high risk for future cardiac events. Thus, dipyridamole cardiac imaging is helpful in the diagnosis of coronary artery disease and in risk stratification.

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It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 +/- 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (% delta L) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

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To assess the efficacy of magnetic resonance (MR) imaging in evaluating graft patency after coronary bypass surgery, 20 patients who had prior surgery (average 5.5 years, range 1.5 to 14) and recent cardiac catheterization because of chest pain were studied. No patient had surgical intervention or change in symptoms in the time interval between catheterization and MR imaging. These 20 patients had a total of 47 grafts, defined as proximal anastomoses: 20 to the left anterior descending or diagonal artery (LAD), 13 to the left circumflex artery marginal branches (LCX), and 14 to the right coronary artery or posterior descending artery (RCA). The patients underwent cardiac and respiratory gated MR scans in a 0.5 tesla magnet with an echo time of 22 msec and two repetitions in a 128 X 256 matrix. In-plane resolution was 2.7 mm. Every patient had a scan in the transaxial plane and some underwent scanning in the sagittal and coronal planes as well. A graft was considered patent by MR when a signal-free lumen was visualized in an anatomic position consistent with that of a bypass graft, had a lumen larger than the native vessels, was seen on more than one slice, and was seen at a level higher than that of the native vessels. If a known graft was not seen it was considered occluded. The scans were interpreted by consensus of two physicians aware of the operative but not the cardiac catheterization data.(ABSTRACT TRUNCATED AT 250 WORDS)

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Evaluation of myocardial perfusion with thallium-201 SPECT has advantages over planar images. These advantages are related to better contrast of the images, lack of superimposition of normal and abnormal areas, and a three-dimensional representation of the site and extent of perfusion abnormalities (ischemia, scar, or both). For this reason, rotational tomography is superior to planar imaging in assessing the extent of coronary artery disease, in the detection of small infarcts, and for quantitative measurements. Several techniques have provided accurate quantitative data for infarct sizing both in animals and men. The ability to quantitate infarct size (or ischemia) will be extremely important in studies of myocardial salvage, risk stratification, and longitudinal studies to evaluate the effects of medical and surgical interventions.

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In a study to test the hypothesis that vascular reserve is exhausted in the setting of a resting blood flow deficit, the left anterior descending or circumflex artery was cannulated and perfused from the left carotid artery. After reactive hyperaemia had been assessed a stenosis was produced with a screw clamp. In the first experiment a moderate stenosis (diastolic perfusion pressure 40 mmHg) was produced in the left anterior descending artery (three dogs) or left circumflex artery (three dogs). Blood pressure was held constant with aortic constriction during intracoronary adenosine infusion (6 mumol.min-1). The stenosis was then adjusted to the preadenosine perfusion pressure. In the second experiment the anterior interventricular coronary vein was also isolated and segment length crystals were placed in the ischaemic and non-ischaemic zones. Severe stenosis (flow reduction of at least 50% and evidence of decreased segmental shortening) was produced in the cannulated left anterior descending artery (eight dogs). Intracoronary adenosine was given with aortic pressure held constant by transfusion and coronary venous drainage. In the first experiment resting coronary flow (ml.min-1) decreased from 41(3) to 29(6) (p less than 0.05) with stenosis. Coronary flow increased from 29(6) to 34(7) (p less than 0.05) with adenosine and to 50(10) (p less than 0.05) with stenosis adjustment. Subendocardial flow (ml.g-1.min-1) decreased from 0.89(0.26) to 0.78(0.23) (p less than 0.05) with adenosine and then increased from 0.94(0.49) with perfusion pressure adjustment. Subepicardial flow tended to increase with adenosine, and increased further with stenosis adjustment.(ABSTRACT TRUNCATED AT 250 WORDS)

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