Influence of preload and afterload on stroke volume response to low-dose dobutamine stress in patients with non-ischemic heart failure: a cardiac MR study.

BACKGROUND: Lack of increase in left ventricular (LV) stroke volume (SV) during low-dose dobutamine stress (LDD) is attributed to exhausted cardiac contractile reserve in failing heart. However, the role of the afterload and preload in SV changes is underestimated. The aim of the study was to investigate the effects of LDD on preload reserve and afterload in patients with non-ischemic heart failure. METHODS: 58 patients (age 62 years) underwent LDD (up to 20µg/kg/min) using cardiac magnetic resonance. RESULTS: LV-SV increased by 27% in 24 patients (p<0.001) (SV+), while decreased by 19% in 22 patients (p<0.001) (SV-). The LDD-to-rest reduction in preload, as defined by LV end-diastolic volume (EDV), was more pronounced in SV- than SV+ (24% and 8% respectively, p<0.05). The LLD-to-rest increase in systolic blood pressure to LV end systolic volume ratio, an index of LV contractility, was higher but not statistically different in SV+ in comparison to SV- (70% vs 48%, p=ns). Systemic vascular resistance during LDD tended to be higher in SV- (23%, p=ns), while it was significantly reduced in SV+ (9.5%, p<0.011), whereas arterial elastance (Ea) increased in SV- (30%, p<0.001) but decreased in SV+ (0.5%, p=0.04). At multivariable regression models LV-EF, LV-EDV and Ea significantly contributed to LV-SV changes in all patients. Also among SV+ and SV- LV-EDV and Ea revealed significant contribution to LV-SV change. CONCLUSIONS: At similar contractile reserve response, the lack of LDD-induced increase in LV-SV, can be related to reduced preload reserve as well as to increased afterload.

The association between the 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor-1 gene and extension of postsurgical calf vein thrombosis.

The objective of this study was to evaluate whether the presence of a plasminogen activator inhibitor type 1 (PAI-1) promoter polymorphism 4G/5G could significantly influence the proximal extension of vein thrombosis in spite of anticoagulant treatment in patients with calf vein thrombosis (CVT) following orthopaedic, urological and abdominal surgery. We studied 168 patients with CVT, who had undergone orthopaedic, urological and abdominal surgery, subdivided as follows: first, 50 patients with thrombosis progression; second, 118 patients without thrombosis progression. The 4G/5G polymorphism of the plasminogen activator inhibitor 1 was evaluated in all patients and in 70 healthy matched controls. We also studied PAI-1 activity in plasma. The presence of 4G/5G genotype was significantly increased in the group of patients with the extension of thrombotic lesions and was associated with an increase in CVT extension risk (odds ratio adjusted for sex 2.692; 95% confidence interval 1.302-4.702). Moreover, we observed a significant increase of PAI-1 plasma activity in patients with extension of thrombotic lesion vs. patients without extension (P=0.0001). Patients with 4G/5G genotype in the promoter of the plasminogen activator inhibitor - 1 gene present a higher risk of extension of thrombotic lesions.

[Combined evaluation of myocardial perfusion and contractility by cardiac magnetic resonance with adenosine stress test: feasibility and accuracy in detecting coronary artery disease]. / Valutazione combinata della perfusione e della contrattilità miocardica mediante risonanza magnetica con stress all'adenosina: fattibilità ed accuratezza nella diagnosi di malattia coronarica.

BACKGROUND: Protocols of cardiac magnetic resonance imaging (CMR) during pharmacological stress with adenosine may include scanning sequences for the evaluation of both myocardial perfusion and contractility. The aim of this study was to define the feasibility and diagnostic accuracy of a stress CMR protocol including the combined evaluation of regional myocardial perfusion and contractility in the identification of patients with significant coronary artery disease. METHODS: A total of 184 consecutive patients with known or suspected coronary artery disease underwent stress CMR (adenosine, 140 microg/kg/min). The employed protocol included the application of the following sequences for image acquisition: 1) cine imaging at rest; 2) perfusion imaging (Gd-DTPA, 0.05 mmol/kg) during pharmacological stress; 3) cine imaging during pharmacological stress; 4) perfusion imaging (Gd-DTPA, 0.05 mmol/kg) at rest. RESULTS: Stress CMR was completed in 182 patients (99%). Minor complications were observed in 12 patients (7%) during adenosine infusion, while one patient developed severe bronchospasm and another patient experienced persistent myocardial ischemia. Good/excellent-quality images were obtained in 91% of stress CMR exams. In a subgroup of 37 patients, when compared with the use of perfusion images alone, combination of perfusion and contractility data provided higher levels of sensitivity (74 vs 89%, p < 0.05) and of negative predictive value (71 vs 85%, p < 0.05) in identifying patients with significant coronary artery disease by invasive angiography. CONCLUSIONS: Adenosine stress CMR including the evaluation of both myocardial perfusion and contractility is feasible and improves diagnostic performance in the recognition of patients with significant coronary artery disease.

Optimal duration of treatment in surgical patients with calf venous thrombosis involving one or more veins.

The aim of this study was to evaluate different durations of treatment in patients with calf venous thrombosis (CVT) involving 1 or more deep veins. The authors studied 2 groups of patients with postsurgical CVT diagnosed by echo-color Doppler. The first group consisted of 68 patients with CVT involving a single vein, and the second group consisted of 124 patients with CVT involving 2 or more veins. Immediately after diagnosis, all patients were treated with nadroparin calcium and sodium warfarin. Heparin treatment was withdrawn after 5-6 days of treatment, when the international normalized ratio (INR) was stabilized between 2 and 3. Each group was divided into 2 subgroups receiving anticoagulation treatment for 6 or 12 weeks, respectively. The endpoint was proximal extension of the thrombotic lesion, defined as the extension of the thrombus to the popliteal and/or femoral vein. In patients with single-vessel CVT there was no significant difference between the 2 subgroups, whereas in patients with CVT involving 2 or more vessels, a statistically significant difference was observed, the number of cases showing proximal extension of the thrombus being higher among patients treated for 6 weeks. Twelve weeks of anticoagulation treatment is better than 6 weeks only in patients with postsurgical CVT involving 2 or more veins.

Efficacy of the treatment with prostaglandin E-1 in venous ulcers of the lower limbs.

BACKGROUND: Venous ulcers represent an important medical problem because of their high prevalence and consequent sanitary costs. In this study, we evaluated the effect of prostaglandin E-1 (PGE-1), a drug that improves district ischemia, on the healing of venous ulcers. METHODS: We performed a randomized, placebo-controlled, single blind study in which 87 patients who had venous leg ulcers homogeneous for dimensions and characteristics were treated for 20 days with an infusion of prostaglandin E-1 or placebo, in association with topical therapy. The dimension and the number of the ulcers were determined at the beginning of the treatment and then every 20 days up to 4 months, or until total recovery. The main outcome of the study was the recovery percentage of the ulcers at the end of the 120-day period of observation and the referred healing time. The reduction in the extension of ulcers from the baseline measurement to the last observation was also evaluated. RESULTS: The baseline characteristics of the treatment and control groups were similar. The reduction in the size of the ulcers was faster in the patients treated with PGE-1. In this group, 100% of the ulcers healed < or = 100 days, whereas in the placebo group, only 84.2% did so by the end of the 120-day observation period (P < .05). The estimated healing times of 25%, 50%, and 75% of the patients treated with PGE-1 were 23, 49, and 72 days, respectively, compared with 52, 80, and 108 for the patients in the placebo group. Only one serious event occurred in the treated group. CONCLUSIONS: This study demonstrates the effectiveness of PGE-1 in reducing the healing time of venous ulcers, suggesting that venous ulcers should also be considered ischemic.

A case of ovarian hyperstimulation syndrome associated with the methylenetetrahydrofolate reductase mutation gene.

OBJECTIVE: To report a case of ovarian hyperstimulation syndrome with methylenetetrahydrofolate reductase (MTHFR) gene 677T homozygosis mutation and A1298C gene heterozygosis mutation. DESIGN: Case report. SETTING: A pregnant woman in an academic hospital. PATIENT(S): A woman with ovarian hyperstimulation syndrome. INTERVENTION(S): Nadroparin was administered for 2 weeks at a dosage of 200 IU/kg twice per day and then once per day; also administered once per day were folates, 5 mg; B6 vitamin, 15 mg; and B12 vitamin, 1 mg. MAIN OUTCOME MEASURE(S): Clinical follow-up. RESULT(S): Delivery was regular within the set time limits, and the fetus was born alive and in good health. CONCLUSION(S): We believe that MTHFR mutation research could be executed in women before ovarian stimulation treatment, but other observations are necessary to support this recommendation.

Subclavian stenosis/occlusion in patients with subclavian steal and previous bypass of internal mammary interventricular anterior artery: medical or surgical treatment?

There are only a few published studies on the association between subclavian steal syndrome and ischemic heart disease. The objective of this report is to evaluate the efficacy of subclavian steno-occlusion treatment in patients with subclavian steal syndrome (SSS) and previous coronary bypass. Over the last 8A years we observed 207 patients who underwent left internal mammary artery-intraventricular artery (LIMA-IVA) bypass graft. Of these, 31 patients were affected by steno-occlusion of the homolateral subclavian artery. Ten patients (group 1) showed latent vertebral-SSS and were pharmacologically treated. Seven patients (group 2) had an intermittent vertebral-SSS; four patients were treated with angioplasty and stent application and three were pharmacologically treated. Fourteen patients (group 3) with complete vertebral-SSS were treated with angioplasty and stent application or carotid-subclavian bypass graft. All patients were followed up every 3 months for a period of 5A years after the diagnosis. The first group of patients showed no angina and no sign of subclavian restenosis. In the second group only two patients, who were affected by angina, showed subclavian restenosis at angiography. In the third group only one patient underwent further angioplasty for restenosis. The results of this study show that the SSS may be an adverse event in patients with a LIMA-IVA bypass graft. Identification of the steal is essential to choose an appropriate therapeutic approach.

Transmural coronary inflammation triggers simultaneous multivessel rupture of unstable plaques.

The authors describe a case of sudden cardiac death caused by the simultaneous multivessel rupture of unstable atherosclerotic plaques, triggered by a transmural inflammatory process (coronaritis). Male subject, 44 years old, apparently in good health until 1 hour before death, when he complained of worsening dyspnea. At autopsy, it was found that the heart weighed 486 g. Evaluation of the coronary arteries revealed the presence of atherosclerotic plaques resulting in a lumen critical stenosis of the left anterior descending artery (LAD), right coronary artery (RCA) and left circumflex artery, and acute occlusive thrombosis of the LAD and RCA. Transverse sections of the ventricular mass highlighted the presence of eccentric hypertrophy of the left ventricle associated with myocardiosclerosis of the posterior interventricular septum and of the posterior wall of the left ventricle. Histology revealed the presence of a coagulative myocytolysis ascribable to the free walls of the left ventricle, and a focus of lymphocytic-active myocarditis. All coronary arteries were sites of intima fibroatheromatous plaques complicated by rupture and thrombosis within the RCA and LAD and by a transmural infiltrate consisting of macrophages and T-lymphocytes associated with consensual medionecrosis and perineuritis. In conclusion, the present case report confirms the hypothesis that inflammation plays a key role in the onset of acute coronary syndromes as it promotes the formation of an unstable plaque as well as its rupture.