Angiology

Background: There has been increasing recognition of the detrimental effect of peripheral arterial disease (PAD) on the health of Americans, and yet there is no common national program of public PAD education designed to diminish this effect.

Format: To heighten awareness of this problem, a 2-day PAD Public Education Strategy Meeting was recently attended by representatives of 17 professional societies and public health associations whose missions support the prevention, diagnosis, treatment, and rehabilitation of vascular diseases. This Public Education Strategy Meeting was intended to provide the rationale and structure to create a national PAD public awareness campaign to diminish the health effect of PAD and to improve cardiovascular outcomes in the United States. This document (1) provides the rationale for creation of a national PAD public education program; (2) reviews the development and success of national hypertension, hypercholesterolemia, and Women’s Heart Health public education programs as models of educational efficacy; (3) elucidates how the work of many vascular professionals has led to a national consensus for creation of a national PAD public educational program; (4) provides an overview of the National Heart, Lung, and Blood Institute PAD education meeting; and (5) outlines the “next steps” required to accomplish these goals.

Outcome: This meeting achieved consensus that we share responsibility for developing accurate, unified messages to promote PAD awareness and improved care. Participants agreed

The aim of this study was to evaluate the prevention of recurrent deep vein thrombosis (RDVT) with an oral antithrombotic agent (sulodexide) in moderate to high-risk subjects. A group of 405 patients was included into the multicenter registry. Both compression and an exercise program were used as well as a risk-factors control plan. After diagnosis of DVT, patients were treated with oral anticoagulants for 6 months. At the end of this period a coagulation study was made and patients started treatment with oral sulodexide capsules for a period of 24 months. The femoral, popliteal, tibial, and superficial veins were scanned with high-resolution ultrasound at inclusion; scans were repeated at 6, 12, 18, and 24 months. Of the 405 subjects included into the registry 178 in the control group (mean age 52.2; SD 11; M:F = 90:88) and 189 in the treatment group (mean age 53.2; SD 10.3; M:F = 93:96) completed the analysis period of 24 months. At 6 and 12 months the incidence of R-DVT was lower (p<0.05) in the treatment group. At 24 months the global incidence of R-DVT was 17.9% in the control group and 7.4% in the sulodexide group (p<0.05), 2.42 times lower than in controls. The 2 groups were comparable for age and sex distribution and for the localization of the thrombi at inclusion. Also the 2 groups of dropouts were comparable. In the control group there were 32 recurrent DVTs and 24 subjects lost to follow-up (total of 56) of 202 included subjects (27.7%) in comparison with 28 failures (14 recurrent DVTs and 14 lost subjects) of 203 subjects (13.8%) in the treatment group. This difference was statistically significant. In this analysis the incidence of DVT in controls was 2.07 times higher than in the treatment group subjects. In conclusion sulodexide was effective in reducing recurrent thrombotic events in high-risk subjects.

This is a study of 97 patients who underwent 106 femoropopliteal bypass grafts (9 bilateral bypasses) for short-distance claudication and critical ischemia. Patients were divided into 2 groups. The first group (n=64) was followed up by use of duplex scans. The second group (n=42) was followed up in clinic without duplex surveillance. Twenty-three patients from the surveillance group developed stenoses of the grafts. Of these, 14 underwent successful angioplasty. A total of 43 grafts became blocked. Graft occlusion was significantly more common in the nonsurveillance group (n=29) as compared to the surveillance group (n=14) after both 1 and 3 years of observation (p=0.001). Patients with critical ischemia showed a higher rate of graft occlusion than the claudicants (p=0.0075). Sixteen patients in the nonsurveillance group underwent above/below-knee amputation compared to 1 in the surveillance group. There was no significant difference in the mortality rate in the 2 groups. Graft surveillance helped to improve patency of grafts by identifying the correctable lesions.

This study was designed to assess the circadian variation of the efficacy of thrombolytic therapy (TT) in 163 patients with acute myocardial infarction. Statistical analysis of the results suggests the existence of circadian variation in the efficacy of thrombolytic therapy with marked early morning resistance and significantly better late daytime results. There is a strong relationship between the normal physiologic rhythms of biochemical, hemodynamic, and hematologic parameters, observed in patients with CAD and the circadian fluctuations of efficacy of TT. Obviously the efficacy of TT is influenced by more evident impact of chronorisk factors during the early morning hours.

Recent epidemiologic studies have shown that moderately elevated plasma homocysteine concentrations are associated with an increased risk for the development of atherosclerotic cardiovascular diseases. But, it is not known whether moderate hyperhomocysteinemia is associated with the angiographic extent of atherosclerotic cardiovascular disease in patients with coronary artery disease (CAD). A possible relationship was investigated between admission plasma homocysteine level and the angiographic extent of coronary artery disease in patients with CAD. In this study, 156 consecutive patients presenting with coronary artery disease (group 1) and control group (group 2) of 35 age-matched persons with normal coronary angiography were enrolled. Blood samples for homocysteine were obtained on admission. Plasma homocysteine concentration was measured with high-performance liquid chromatography with fluorescence detection. Radiographs from coronary angiography were viewed and scored using Sullivan’s method to assess the atherosclerotic involvement of coronary artery disease. There were significant elevations in homocysteine level in group 1 compared to group 2 (15.59 ±5.7 µmol/L, 9.24 ±1.50 µmol/L; respectively, p<0.001). All scores (demonstrated angiographic extension of CAD) correlated significantly with plasma homocysteine levels; however, the Sullivan’s extent score correlated more closely (r =0.68, p<0.001) than both the stenosis score (r =0.44, p<0.01) and vessel score (r =0.35, p<0.05). Elevated homocysteine levels in patients with coronary artery disease correlated with the angiographic extent of atherosclerotic disease.

The goals of this study were to determine the value of the isoproterenol (ISO) head-up tilt (HUT) test in detecting coronary vasospastic angina and to investigate the possible mechanism responsible for coronary artery spasm. The ISO + HUT test was performed in 16 patients with coronary artery spasm documented by the intracoronary ergonovine provocation test. Patients’ blood pressure and heart rate were measured at baseline, during the ISO + HUT (phase I), and during HUT after discontinuation of ISO (phase II). Patients were categorized as test-positive if they developed angina with ST-segment elevation during testing. Eight patients (50%) were test-positive (5 in phase I and 3 in phase II). Between the test-positive and test-negative groups, no significant differences were noted in the changes in blood pressure throughout the test. However, there were significant differences in the changes in heart rate from supine to 2 minutes after HUT under ISO infusion (-17 ±22 vs 11 ±25 beats/minute; p=0.035). In those patients with a positive result in the phase I stage, the heart rate decreased initially after tilt-up, and then significantly increased later (from 85 ±16 to 110 ±27 beats/minute; p=0.043), when coronary vasospasm occurred. In those patients with a positive result in the phase II stage, coronary vasospasm occurred immediately after HUT, when there was an insignificant transient increase in heart rate from the supine to the HUT position (from 85 ±12 to 92 ±11 beats/minute; p=0.109). The ISO + HUT test can provoke coronary vasospasm with ST-segment elevation in 50% of the patients with coronary artery spasm, when combined with an extensional protocol of HUT after discontinuation of ISO. This study suggests that the induction of coronary artery spasm during HUT testing is associated with a rapid elevation of sympathetic activity during augmented parasympathetic activity.

Increased intima-media thickness (IMT) in the common carotid artery (CCA) correlates with conventional risk factors for cardiovascular disease and is an independent predictor of cardiac events. However, correlation between IMT and degree of ischemic heart disease evaluated by coronary angiogram is weak. The purpose of this study was to investigate the relationship between measures of carotid atherosclerosis and the extent and severity of coronary artery disease (CAD) in 111 consecutive patients (60 men and 51 women, mean age 60 years) with known or suspected CAD who were investigated with adenosine-stress myocardial perfusion scintigraphy. Common carotid artery lumen diameter (LD) and IMT of the carotid bulb and distal CCA were measured with ultrasound, and CCA cross-sectional intima-media area (CIMA) was calculated. Seventy-two of 110 patients (65%) had significant perfusion defects. Increasing carotid plaque occurrence (absence, unilateral or bilateral occurrence) correlated with more advanced CAD (p<0.01). The extent and severity of myocardial hypoperfusion correlated significantly with presence of carotid plaque (r =0.23 and 0.24 respectively, p<0.05), CIMA (r =0.23 and 0.22, p<0.05), and LD (r =0.26 and 0.25, p<0.01) but not with IMT. In contrast to CIMA, LD failed to show an independent relation to extent of CAD after adjustment for age, sex, and body mass index. In conclusion, in subjects with intermediate to high risk of ischemic heart disease, occurrence of carotid plaques and increased cross-sectional intima-media area in the common carotid artery are the best parameters for predicting CAD expressed as myocardial hypoperfusion.

Growing evidence suggests that atherosclerosis is an immune-mediated inflammatory process and that cytokines participate as mediators in this process. Of the cytokines, interleukins, which are released from both immune and nonimmune cells of vascular wall, are found to have multiple effects. Interleukin-2 (IL-2), a cytokine produced by activated T-lymphocytes, has been found to further activate the T cells and may potentially enhance atherogenesis. Apo-E-deficient mice fed with atherogenic diet were injected intraperitoneally twice a week with placebo, IL-2, or anti-IL-2 antibody for a period of 6 weeks. Group 1 (n=6) was injected with bovine serum albumin (BSA) in phosphate-buffered saline (PBS) and served as controls. Group 2 (n=6) was injected with 2x10⁴ units of recombinant murine IL-2 (rmIL-2) per dose reconstituted with BSA in PBS. Group 3 (n=6) was injected with 5 µg of anti-IL-2 per dose reconstituted with BSA in PBS. Aortic sections were analyzed and atherosclerotic burden was quantified. Compared to controls, injection of IL-2 increased measures of atherosclerosis such as the average lesion score (10.7 ±0.5 vs 9.3 ±1.1, p=0.04) and the lesion size as a fraction of aortic area (0.51 ±0.03 vs 0.41 ±0.05, p=0.01). Injection of anti-IL-2 had a profound antiatherogenic effect. It significantly reduced the average number of lesions per cross section (2.6 ±0.6 vs 4.3 ±0.6, p=0.03), the average lesion score (4.6 ±1.9 vs 9.3 ±1.1, p=0.02), the lesion area/circumference (0.35 ±0.08 vs 0.62 ±0.10, p=0.007), and the lesion size/aortic area (0.23 ±0.07 vs 0.41 ±0.05, p=0.03). These results indicate that IL-2 is an atherogenic cytokine in apo-E-deficient mice and anti-IL-2 is protective against atherosclerosis. This may have important clinical implications in modifying the atherosclerotic process.

Basal septal hypertrophy (BSH), a cause of left ventricular outflow tract (LVOT) obstruction, is thought to occur by increased ventricular dynamics. The aim of the study was to evaluate the effect of pharmacologic stress on LVOT gradients in a group of hypertensive patients with BSH. Dobutamine stress was used in 24 hypertensive patients (mean age 56 ±8 years; 11 women) with BSH and 20 normal controls (mean age 54 ±9 years; 7 women). Ejection fraction and myocardial mass, basal septal dimension, and LVOT diameter were measured with 2-dimensional echocardiography. LVOT velocities and transmitral velocities before and at peak dobutamine infusion were determined by continuous wave Doppler and pulsed Doppler, respectively. There were no differences in mean ejection fraction and myocardial mass between BSH patients (58 ±3%, 204 ±24 g) and normals (56 ±4%, 201 ±32 g). The basal septum was thicker in patients (1.55 ±0.2 cm) than in normals (1.03 ±0.1 cm, p<0.001). Maximum LVOT velocities were similar in BSH (1.2 ±0.4 m/sec) and normals (1.1 ±0.2 m/sec) at rest. At peak stress, maximum LVOT velocities were higher in BSH (3.3 ±0.6 m/sec) than normals (1.7 ±0.4 m/sec, p<0.001). LV rate-pressure product at peak stress was higher in BSH (23,326 ±4,388) than normals (17,592 ±2,409, p<0.001). LV isovolumetric relaxation time was prolonged, and the E/A ratio was decreased in the patients at rest (130 ±14 msec and 0.72 ±0.18, respectively, p<0.001). At peak stress, diastolic function did not significantly change in two groups. The correlations between LVOT velocity change by stress and mean LVOT diameter (r =-0.668, p<0.001) and mean BS thickness (r =0.610; p<0.001) were significant in the whole group. High velocities appeared on LVOT at peak pharmacologic stress in the hypertensive patients with BSH compared with control group. This suggests dynamic ventricular ejection by stress may contribute to hypertrophy of the basal segment, which is the closest part of septum to increased afterload.

There are varying reports on the electrocardiogram in pericardial effusions. Some correlate low QRS voltage with tamponade and the size of the effusion while others do not. Low voltage also appears to vary with the etiology. There are no reports on the influence of pericardial thickness or changes in the P voltage. The authors studied 43 patients with large effusions of whom 26 had tuberculosis and the remaining had viral/idiopathic etiology. Pericardial thickness was measured at chest computed tomography. They found no correlation between the low QRS voltage and tamponade, size of the effusion, etiology, or pericardial thickness. Low voltage of the P wave and T-wave changes were more frequent than low QRS voltage.

Spontaneous coronary artery dissection is rare, but is now being increasingly recognized as a prominent cause of acute ischemic coronary events occurring usually in relatively young patients, predominantly females. The authors describe the clinical course of 3 patients (1 woman) in whom large spontaneous coronary artery dissections developed. All had diverse clinical presentations; 1 presenting with heart failure, the second with post-myocardial infarction angina, and the third with syncope. The second patient underwent coronary angioplasty with multiple overlapping stents while in the other two, it was the considered opinion to continue aggressive medical therapy. The 1-year follow-up was uneventful in all 3 patients. The risk factors ascertained in our patients were diabetes mellitus, smoking, and hypertension.

Essential thrombocythemia is a clonal disorder of the myeloid stem cell that causes pathologic expansion of the megakaryocytic elements in the bone marrow, with a persistent increase in the platelet count. The disease is associated with an elevated risk of thrombosis, hemorrhage, and vasomotor symptoms. The presenting features of essential thrombocythemia can range from being asymptomatic to thrombohemorrhagic complications including acute myocardial infarction. Acute ST-segment elevation myocardial infarction due to left main trunk and ostial left anterior descending coronary artery lesions was diagnosed in a young 31-year-old man. Platelet count was markedly increased and essential thrombocythemia was also diagnosed. Because of left main disease, primary coronary intervention was not feasible and an emergent coronary artery bypass grafting was performed along with pharmacologic management of essential thrombocythemia. The early postoperative period was complicated by acute pulmonary embolism. Hydroxyurea and anagrelide were administered postoperatively, resulting in the decrease of platelet count. A succinct review of myocardial infarction in patients with essential thrombocythemia is presented, and therapeutic strategies in such patients are discussed.

Three cases of spontaneous arteriovenous fistulas of the vertebral artery (VAF) are reported. In one case the only symptom was a cervical bruit; in the other two cases, symptoms of multiple cervical radiculopathy were also observed. Definitive diagnostic findings were obtained by Doppler ultrasonography, computed tomography, magnetic resonance imaging, and angiography. Clinical signs of radiculopathy disappeared after endovascular balloon occlusion of the fistula, in about 1 month. In one case the vertebral artery was occluded without clinical consequences.

Familial hypercholesterolemia (FH) is a relatively common autosomal monogenic disease with dominant inheritance and threefold to fourfold increase in relative risk of cardiovascular death in untreated patients. For a “definitive” clinical diagnosis of FH the Simon Broome Register proposes the presence of tendon xanthomas as a key feature. However, detection of tendon xanthomas by physical examination is subjective and difficult to use for follow-up purposes. Several instrumental methods have been reported to be more sensitive than physical examination for the evaluation of xanthomas. The present case illustrates the usefulness of computed tomography (CT) to detect xanthomas in the Achilles tendons (XAT) and their regression in response to hypolipidemic drug treatment in a heterozygous FH patient. As XAT are atherosclerotic plaque-like depositions of lipids it is likely that their progression or regression follows the behavior of vascular atherosclerotic lesions.

Prostacyclin treatment successfully delays the need for lung transplantation in many patients with progressive primary pulmonary hypertension by vasodilating pulmonary arteries. However, the treatment of pulmonary hypertension with prostacyclin may cause a paradoxical increase in pulmonary artery pressure, as shown in this case.

This case report highlights the emergence of new complications associated with old procedures as the frequency of their use increases. A 29-year-old man with aplastic anemia was admitted for a bone marrow transplant. Before this procedure, a Hickman line was inserted. This was followed by hoarseness of voice. An examination revealed an immobile left vocal cord. Further investigations did not show any cause for this complication. Therefore, the hoarseness and vocal cord paralysis was attributed to trauma associated with the insertion of the Hickman line.