Angiology

Enhanced external counterpulsation (EECP) is an effective noninvasive treatment for coronary artery disease. The mechanism of action is felt to be hemodynamic. The complex hemody namic effects have been simply quantified by calculating a previously described effectiveness ratio (ER).

The EECP Clinical Consortium, a clinical registry of 37 centers, prospectively enrolled 395 chronic stable angina patients (79 women, 316 men, mean age 66 years) to examine the relation of the ER to posttreatment improvement in Canadian Cardiovascular Society angina class (CCS). Women and the elderly underwent planned subgroup analysis. The ER was calcu lated during the first and last hours of a 35-hour course of EECP treatment.

After EECP, CCS improved by at least 1 class in 88% of patients, 87% of men and 92% of women (p = NS), and in 89% of patients ≤ 66 years and 88% of patients > 66 years old (p = NS). The initial and final ER were similar in patients with and without improvement in CCS. Significant first-hour ER differences were seen between men and women (0.96 ±0.03 vs 0.76 ±0.04, p < 0.005), and between ages ≤ 66 and > 66 years old (1.04 ±0.04 vs 0.81 ±0.03, p < 0.0001). However, all subgroups responded equally well to EECP treatment.

EECP is effective in improving CCS in chronic stable angina patients; it has comparable effects in men and women and across a broad range of ages. The hemodynamic effect of EECP (ER) does not predict improvement in CCS and may indicate that other factors, such as neuro- hormonal changes, may have a significant role in mediating the observed EECP benefits.

The long-term outcome of primary successful percutaneous transluminal angioplasty (PTA) for patients with peripheral occlusive arterial disease (POAD) is frequently compromised by the development of restenosis, especially when extensive dissections result from the angioplastic procedure. Unfortunately, prevention of the occlusive process by means of drugs such as antithrombotics, anticoagulants, thrombolytics, corticosteroids, lipid reducers, or cytostatics has not been demonstrated convincingly. The authors sought to clarify whether such patients could benefit from the postsurgical administration of low-molecular-weight heparin.

A total of 172 POAD patients with extensive dissections after PTA in the pelvic or upper leg regions were randomized for 7-day post-PTA intravenous treatment with either full heparinization or nadroparin calcium followed by adjunctive oral aspirin for 6 months. The primary outcome measure was the degree of stenosis (normal findings; stenosis <50%, > 50%, >80%, occlusion) before and after angioplasty, as well as 3 weeks and 3 and 6 months after dilation; secondary efficacy criteria included changes in the Fontaine stage and in the cruro brachial ratio.

No significant treatment-related differences were found at the 3 post-PTA follow-up exam inations with regard to the degree of stenosis. This was also the case for the subgroup of patients (n = 62) who had undergone angioplasty in the pelvic region. By contrast, when angio plasty was performed in the superficial femoral artery (n = 110), the degree of restenosis was significantly lower (p<0.01) among patients receiving nadroparin calcium compared to those given heparin at week 3, month 3, and month 6. No intergroup differences emerged for secondary outcome measures in the long term or for safety parameters. These preliminary results indicate that patients with extensive dissections after PTA treatment for POAD in the upper leg region might benefit from a reduction in the rate of restenosis by administration of 7-day weight-adjusted nadroparin calcium.

This study was undertaken to evaluate the pathophysiologic and clinical effects of the early application of percutaneous transluminal coronary angioplasty (PTCA) supported by stenting on non-Q-wave myocardial infarction (MI). Ninety-four patients with non-Q-wave MI and 316 patients with Q-wave MI were studied. Early PTCA with provisional stenting (40%) was performed in all of them. A history of MI (22% vs 12%, p=0.018), preinfarction angina ≤24 hours before the onset of MI (60% vs 33%, p<0.001), and patent infarct-related vessels (83% vs 21 %, p<0.001) were significantly more common in non-Q-wave MI than in Q-wave MI. As predictors of the occurrence of non-Q-wave MI, preinfarction angina (p = 0.00 1 ) and previous MI (p=0.021) were significant variables. Clinical outcomes showed more improvement in in- hospital death (0.0% vs 5.0%, p = 0.036) and long-term event-free curves for death and/or MI (p = 0.035) in non-Q-wave MI than Q-wave MI when patients with previous MI were excluded. There was no significant difference in clinical outcome between the two groups when patients with previous MI were included. The high incidence of patent infarct-related vessels and prein farction angina as well as the improved outcome obtained by early PTCA/stenting suggest instability of coronary occlusion and culprit coronary lesions in non-Q-wave MI. In conclusion, non-Q-wave MI constitutes a characteristic feature of MI induced by unstable coronary lesions, and early interventional therapies are presumed to result in improved outcomes by stabilizing the unstable culprit lesions.

The progressive increase of deaths and morbidity from cardiovascular disease (CVD) in most developed societies has led to the formulation of preventive strategies and application of several diagnostic guidelines. However, there is emerging evidence that most panels and algo rithms are inadequate and require urgent revision and updating. Therefore, the aim of this study was the evaluation of a wide cardiovascular risk profile in elderly male patients with acute myocardial infarction (AMI) or peripheral occlusive disease (POD). The risk profile was assessed by measuring conventional serum lipid and lipoprotein levels and emerging parame ters : lipoprotein(a) (Lp[a]), homocysteine (Hcy), and C-reactive protein (CRP).

The concentration of triglycerides, Lp(a), Hcy and the total cholesterol/high-density lipoprotein (TC/HDL) ratio were significantly higher in both classes of patients than in a popu lation of matched healthy controls and, similarly, patients with CVD displayed lower plasma values of HDL. No significant differences were observed for TC, low-density lipoprotein (LDL), and CRP. Patients with POD exhibited a marked atherogenic profile, as attested by substan tially increased values of Hcy, Lp(a), triglycerides, and TC/HDL ratio. The frequency distribu tions of Lp(a) and Hcy concentrations were markedly shifted toward upper values in both classes of patients than in controls. In multivariate regression analysis, Lp(a) and Hcy were the best predictors for AMI, whereas Lp(a), Hcy, and the TC/HDL ratio were the best predic tors for POD. Taken together, these data suggest that Lp(a) and Hcy excesses might exert a central role in the development of atherosclerotic disease in elderly male patients. Thereby, the inclusion of those tests, along with the TC/HDL ratio and other more conventional analyses in panels for the evaluation of the cardiovascular risk might be profitable in terms of effectual prevention.

This study was designed to assess a possible correlation between flow-mediated endothe lium-dependent vasodilation in the popliteal artery and the intima-media thickness of the common carotid artery. Impaired vasodilation is one of early markers of atherosclerosis that has not been studied on the popliteal artery. An increase in intima-media thickness of the common carotid artery is also considered to be an indication of early stages of atherosclerosis. With use of ultrasound, the diameter of the popliteal artery was measured at rest and during reactive hyperemia after 5-minute arterial occlusion. Subsequently, the intima-media thickness was measured in left common carotid arteries in 27 patients with hyperlipidemia, in 10 patients with confirmed coronary artery disease, and in 20 healthy individuals. In healthy individuals, popliteal artery diameter increased by mean of 6.6 ±3.5% (p<0.01) in relation to hyperemia. In patients with hyperlipidemia before therapy and in patients with coronary disease, no increase in diameter occurred (mean, 0.44% and -1.6%, respectively). The difference between healthy individuals and patients was statistically significant at p<0.001. The popliteal artery seems to respond similarly to the brachial artery. When comparing the change in popliteal artery diameter and intima-media thickness of common carotid arteries, a strong negative correlation (r = -0.5713, p < 0.001) was observed in all subjects.

The study was planned to evaluate renal vascular resistance by means of duplex Doppler ultra sonography in patients with progressive systemic sclerosis (PSS) with or without signs of renal involvement. Twenty-two female patients with PSS (mean age 38.5 ± 17.3 years) and 20 age-matched (mean age 36.7 ±7.2 years) female healthy controls participated to the study. Doppler indices of renal vascular resistance—resistive index (RI), pulsative index (PI), and systolic-to-diastolic flow velocities ratio (S/D ratio)—were determined on main renal artery and interlobar artery. RI, PI and S/D ratio were found to be increased in PSS patients with signs of renal involvement as compared to those without renal manifestations and healthy controls (p<0.0001 for all groups). Doppler indices of renal vascular resistance were closely related to the duration of the disease, age, and plasma renin activity. Doppler ultrasound is a useful and informative technique in the monitoring of PSS patients with renal involvement.

The aim of this study is to investigate the value of hemodynamic changes induced by carotid sinus massage (CSM) on the diagnosis of coronary artery disease (CAD). A total 108 patients (mean age, 54 ±10 years, range 33-70) who had no significant stenosis in the carotid artery by duplex ultrasonography (USG) and no history of syncope were included in this study. Carotid sinus massage was performed before coronary angiography with monitoring of electrocardio graphy and blood pressure. The patients were divided into three groups according to response to CSM: group 1 patients had a decrease in blood pressure or < 10 beats/minute (bpm); group 2 patients had a decrease between 10 and 20 bpm; and group 3 patients had >20 mm Hg decrease in blood pressure or > 20 bpm. Coronary angiography was performed after CSM in all patients. There was single-vessel disease (VD) in 23 cases, two-VD in 24 cases, and three-VD in 35 cases. Coronary angiography results were normal in 26 cases. The changes in systolic and diastolic blood pressures and heart rate before and after CSM correlated with number of VD. These changes were highest in patients with three-VD, but lowest in patients with normal coronary angiography. The number of diseased vessels and total coronary artery score were lowest in group 1, but highest in group 3. The specificity and sensitivity of CSM-induced > 10 mm Hg in blood pressure (BP) or > 10 bpm changes in heart rate in the diagnosis of CAD were 85% and 71 %, respectively. The positive and negative predictive values were 93% and 49%, respectively in the diagnosis of CAD. At the end of this study, we concluded that CSM induced the fall in blood pressure and heart rate and was correlated with number of diseased vessels and the score of coronary artery disease. As dichotomized values, the decrease of > 10 mm Hg in blood pressure and/or >10 bpm has highest specificity, sensitivity, and positive predictive value in the diagnosis of CAD.

Treatment of critically ill patients who have heparin-induced thrombocytopenia and throm bosis (HITT) and also renal failure is a challenge. Recombinant hirudin (Refludan, Hoechst Marion Roussel) is a direct thrombin inhibitor indicated for anticoagulation in HITT and approved by the United States Food and Drug Administration. Because this drug is renally cleared, a single dose of hirudin may induce prolonged (up to one week) unpredictable antico agulation in patients with renal insufficiency. There are a few case reports of patients with renal failure and suspected heparin-induced thrombocytopenia (HIT) in which patients were anticoagulated with Refludan for catheter thrombosis. There is no literature on the thera peutic use of Refludan to treat HITT in patients with diffuse thrombosis and renal failure. The authors report the case of a 44-year-old female dialysis patient with HITT and extensive life- threatening thrombosis. The patient developed common iliac vein occlusion extending to the right atrium with progressive right internal jugular vein thrombus developing while on heparin. Her platelet count dropped to 60,000/μL. She was lethargic and hemodynamically unstable. Refludan was initially given as a bolus of 0.2 mg/kg (total, 12 mg) at a 50% dose reduction based on the patient's ideal body weight. This dose was based on the published pharmacoki netics of Refludan in patients with renal failure. Only 2 additional boluses of 6 mg and 3 mg were needed to extend the duration of therapeutic anticoagulation (measured by PTT) to 140 hours. The patient improved both clinically and radiographically after the treatment with Refludan. There were no additional thromboembolic events or bleeding complications. The platelets returned to normal within a few days. The patient was transitioned to coumadin and discharged from the hospital. She remains stable at 1-year follow-up.

Acute embolic renal infarction is an entity that is often misdiagnosed as a renal calculus because of similar presenting symptoms. This leads to delay in the initiation of treatment and to increased morbidity. Few case reports exist relating cardiac emboli to acute renal infarction. The authors present a patient with a renal embolism secondary to left ventricular thrombus. A brief review of the literature highlighting the importance of clinical suspicion in making an accurate diagnosis, the utility of various diagnostic studies, and comparison of various treatment options is presented.

Congenital interruption of the inferior vena cava is an uncommon vascular anomaly. In this setting, the appearance of deep vein thrombosis is very rare because associated azygous or portal continuation develops as a collateral system for venous return. The authors present a case of infrahepatic interruption of the inferior vena cava in a 21-year-old man who presented with symptoms of deep vein thrombosis. Clinical features and prognosis of this entity are discussed.