Search

Background We previously demonstrated that bariatric surgery (BS) leads to a short-term significant improvement of endothelial function and coronary microvascular function. In this study we assessed whether BS maintains its beneficial effect at long-term follow up. Design We studied 19 morbidly obese patients (age 43 ± 9 years, 12 women) without any evidence of cardiovascular disease who underwent BS. Patients were studied before BS, at 3 months and at 4.0 ± 1.5 years follow up. Methods Peripheral vascular function was assessed by flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD), i.e., brachial artery diameter changes in response to post-ischemic forearm hyperhaemia and to nitroglycerin administration, respectively. Coronary microvascular function was assessed by measuring coronary blood flow (CBF) response to intravenous adenosine and to cold pressor test (CPT) in the left anterior descending coronary artery. Results Together with improvement of anthropometric and metabolic profile, at long-term follow-up patients showed a significant improvement of FMD (6.43 ± 2.88 vs. 8.21 ± 1.73%, p = 0.018), and CBF response to both adenosine (1.73 ± 0.48 vs. 2.58 ± 0.54; p < 0.01) and CPT (1.43 ± 0.30 vs. 2.23 ± 0.48; p < 0.01), compared to basal values. No differences in vascular end-points were shown at 3-month and 4-year follow-up after BS. Conclusions Our data show that, in morbidly obese patients, BS exerts beneficial and long lasting effects on peripheral endothelial function and on coronary microvascular dilator function.

In this study, we assessed whether any abnormalities in coronary microvascular and peripheral vasodilator functions are present in patients with variant angina (VA) caused by epicardial coronary artery spasm (CAS).

Classical anti-ischemic drugs are the first-line form of treatment in patients with microvascular angina (MVA), but they often fail to achieve a satisfactory control of angina symptoms. It is unknown whether there is any relation between improvement of angina status and changes in microvascular function induced by classical anti-ischemic drugs in MVA patients.

A growing amount of data is increasingly showing the relevance of coronary microvascular dysfunction (CMVD) in several clinical contexts. This article reviews techniques and clinical investigations of the main noninvasive and invasive methods proposed to study coronary microcirculation and to identify CMVD in the presence of normal coronary arteries, also trying to provide indications for their application in clinical practice.

We investigated whether children with a previous Kawasaki disease (KD) have evidence of abnormal vascular and/or platelet function. We included 14 patients with previous KD and 14 matched controls. We assessed endothelial function by flow-mediated dilation (FMD), carotid intima-media thickness (cIMT), coronary microvascular function by coronary blood flow response (CBFR) to cold pressor test, and platelet reactivity by measuring monocyte-platelet aggregates (MPAs) and CD41-platelet expression by flow cytometry. No differences were found between the groups in FMD, cIMT, or CBFR to cold pressor test. The MPAs were similar in patients with KD and controls. CD41-platelet expression, however, was significantly increased in patients with KD compared with controls, both at rest (14.3 ± 1.9 vs 12.4 ± 1.9 mean fluorescence intensity [mfi], P = .01) and after adenosine diphosphate stimulation (19.3 ± 1.3 vs 17 ± 1.7 mfi, P < .001). In conclusion, children with a previous episode of KD showed increased platelet activation, compared with healthy participants despite no apparent vascular abnormality at follow-up.

To assess the effect of ranolazine on systemic vascular function in patients with type II diabetes mellitus (T2DM).

OBJECTIVES: We assessed whether exercise stress test (EST) results are related to the presence of coronary microvascular dysfunction (CMVD) in patients undergoing elective percutaneous coronary intervention (PCI). BACKGROUND: Previous studies showed that EST is poorly reliable in predicting restenosis after PCI; some studies also showed CMVD in the territory of the treated vessel. METHODS: We studied 29 patients (age 64±6, 23 M) with stable coronary artery disease and isolated stenosis (>75%) of the left anterior descending (LAD) coronary artery, undergoing successful PCI with stent implantation. EST and assessment of coronary microvascular function were performed 24h, 3months and 6months after PCI. Coronary blood flow (CBF) response to adenosine and to cold-pressor test (CPT) was assessed in the LAD coronary artery by transthoracic Doppler echocardiography. RESULTS: Patients with ST-segment depression ≥1mm at EST performed 24h after PCI (n=11, 38%) showed a lower CBF response to adenosine compared to those with negative EST (1.65±0.4 vs. 2.11±0.4, respectively, p=0.003), whereas the difference in CBF response to CPT was not significant (1.44±0.4 vs. 1.64±0.3, respectively; p=0.11). At 3-month and 6-month follow-up a positive EST was found in 12 (41%) and 13 (44%) patients, respectively; patients with positive EST also had lower CBF response to adenosine compared to those with negative EST (3months: 1.69±0.3 vs. 2.20±0.3, respectively; 6months: 1.66±0.2 vs. 2.32±0.3, respectively; p<0.001 for both). CONCLUSIONS: Positive EST after elective successful PCI consistently reflects impairment of hyperemic CBF due to CMVD, which persists over a follow-up period of 6months.

Atrial fibrillation is the most frequent cardiac rhythm disturbance, with prevalence increasing with age. This disease is a major risk factor for ischaemic stroke. The costs resulting from atrial fibrillation are really impressive. Pharmacological agents are the first line therapy for the management of atrial fibrillation. Antiarrhythmic drugs are used to terminate arrhythmias, as acute treatment for conversion of recent onset atrial fibrillation, and to maintain sinus rhythm, as chronic therapy for prevention of atrial fibrillation recurrences. Among antiarrhythmic agents, drugs that inhibit early sodium current (as propafenone) are proven effective in atrial fibrillation. In this review, the most relevant data on propafenone are provided.

BACKGROUND AND AIMS: To assess the effects of bariatric surgery (BS) on peripheral endothelial function and on coronary microvascular dilator function. METHODS AND RESULTS: We studied 50 morbidly obese patients (age 38 ± 9, 13 M) who underwent BS and 20 comparable obese controls (age 41 ± 11, 6 M) without any evidence of cardiovascular disease. Peripheral vascular dilator function was assessed by brachial artery diameter changes in response to post-ischemic forearm hyperaemia (flow-mediated dilation, FMD). Coronary microvascular function was assessed by measuring coronary blood flow (CBF) velocity response to i.v. adenosine and to cold pressor test (CPT) in the left anterior descending coronary artery by transthoracic Doppler echocardiography. The tests were performed at baseline and at 3-month follow-up. At baseline, FMD and CBF response to adenosine and CPT were similar in the 2 groups. Compared to baseline, FMD at follow-up improved significantly in BS patients (5.9 ± 2.7% to 8.8 ± 2.4%, p < 0.01), but not in controls (6.3 ± 3.2% vs. 6.4 ± 3.1%, p = 0.41). Similarly, a significant improvement of CBF response to adenosine (1.63 ± 0.47 to 2.45 ± 0.57, p < 0.01) and to CPT (1.43 ± 0.26 to 2.13 ± 0.55, p < 0.01) was observed in BS patients but not in controls (1.55 ± 0.38 vs. 1.53 ± 0.37, p = 0.85; and 1.37 ± 0.26 vs. 1.34 ± 0.21, p = 0.48, respectively). The favourable vascular effects of BS were similar independently of the presence and changes of other known cardiovascular risk factors and of basal values and changes of serum C-reactive protein levels. CONCLUSIONS: Our data show that, in morbidly obese patients, together with peripheral endothelial function, BS also improves coronary microvascular function. These effects suggest global improvement of vascular function which can contribute significantly to the reduction of cardiovascular risk by BS reported in previous studies.

Background. Venous return and right atrial pressure are increased by clinostatism and by the intrathoracic negative pressure during obstructive sleep apneas. In presence of a interatrial defect this may results in right-to-left shunt. Case report. A 51-yrs obese male was admitted to the cardiology department of our hospital for evaluation of arrhythmias and exertional dyspnoea. He was also referred to the Respiratory unit because of dry mouth and sore throat upon awakening, daytime sleepiness and fatigue, snoring, restlessness during sleep, with a story of wheezing and recurrent bronchitis for years. He had a history of former smoking (20pack/yrs) and a prolonged occupational exposure to wheat. Lung function tests documented a mild chronic obstructive pulmonary disease and high values of the carbon monoxide transfer coefficient. Arterial blood gas analysis in ambient air and in spontaneous breathing was normal. A nocturnal cardiorespiratory polygraphy (CRP) documented a severe pattern of obstructive sleep apnoea syndrome (OSAS) (AHI=83/h, ODI=71/h), with hypoxemia (time with SpO2<90%=89%, <80%=53%). There were different fasis of severe prolonged hypoxemia with superimposed typical apnoeic desaturations (Fig.1). After a short awakening in standing position the hypoxemia recurred after about 1 hour of sleep. The deepest desaturations occurred in both right and left lateral positions. The number of hypo-apnoeic episodes was similar in both normoxemic and hypoxemic phases. The distribution of hypoxemia showed a bimodal pattern (Fig.2). A chest TC scan showed signs of COPD and air trapping during the expiratory phase, with no abnormal findings in the pulmonary circulation. A transthoracic ecocardiography documented a suspected interatrial right-to-left shunt with normal values of pulmonary artery systolic pressure (20 mmHg). A transesophageal ecocardiography confirmed the presence of an interatrial right-to-left shunt which occurred only during deep inspirations. After a

Background: Endothelial dysfunction, reduced coronary flow reserve and increased markers of inflammation are detectable in cardiac syndrome X (CSX). In this study we investigated the relation between inflammation and systemic endothelial function in CSX patients. Methods: We studied 42 CSX patients (55±6 years, 14 men) and 20 healthy subjects (52±7 years, 9 men). Systemic endothelial function was assessed by flow-mediated dilation (FMD) of the brachial artery after 5-minute of forearm cuff inflation. Serum C-reactive protein (CRP) was measured by a high-sensitivity method. Results: FMD was significantly lower in CSX patients compared to controls (4.8±4.4 vs. 13.7±4%, p<0.001), whereas CRP levels were higher in CSX patients than in controls (2.7±2.4 vs. 0.7±0.4 mg/L, p=0.001). In CSX patients FMD showed a significant inverse correlation with CRP levels, even after adjustment for potentially confounding variables (r=-0.34, p=0.006). Conclusion: An impaired FMD is detectable in CSX patients, suggesting a generalized abnormality in vascular function. Subclinical inflammation seems to play a significant role in the impairment of endothelium-dependent vasodilator function of these patients.

OBJECTIVES: Arterial hypertension and its pharmacological control are discussed in view of the high cardiovascular risk due to lack of target blood pressure achievement. It is, therefore, underlined the need for a highly effective therapy, able to provide protection from organ damage through a marked antihypertensive activity. In addition to this basic property, also compliance of the patient to therapy is needed, in order to avoid that the effects of therapeutic measures should result fruitless. DISCUSSION AND CONCLUSIONS: An answer to this problem appears now offered by a recent class of antihypertensive agents, the angiotensin II receptor blockers (ARBs). Among them valsartan has been described, providing an overview of methodologically adequate clinical studies, evaluating the efficacy, even at long-term, and safety. Valsartan has been compared with other antihypertensive agents of proven efficacy, mainly amlodipine, showing a better clinical profile. A wide room was finally left to the problem of adherence to therapy, whose lack is associated very frequently with marked increases in cardiovascular risk, due to absent or insufficient blood pressure control. This implies significant increases of health costs, as documented in numerous Countries, mainly following the higher need for hospitalization. On the other hand, it is also well documented the pharmacoeconomic benefit associated to ARBs use, particularly with valsartan.

Background:The causes of coronary microvascular dysfunction (CMVD) in patients with cardiac syndrome X (CSX) are largely unknown. Common cardiovascular risk factors (CVRFs) and increased markers of inflammation have been associated with CMVD in some studies, but their role in determining CMVD in CSX patients remains poorly known. Methods and Results: We studied 71 CSX patients (56 ± 9 years, 23 men) and 20 healthy volunteers (52 ± 7 years, nine men). Using transthoracic Doppler echocardiography, coronary microvascular vasodilator function was assessed in the left anterior descending coronary artery as the ratio of diastolic coronary blood flow (CBF) velocity at peak intravenous adenosine administration and during cold pressor test (CPT) to the respective basal CBF velocity values. Common CVRFs tended to be more frequent and C-reactive protein (CRP) levels were higher (P < 0.001) in CSX patients than in controls. Both CBF responses to adenosine (2.05 ± 0.6 vs. 2.92 ± 0.9, P < 0.001) and to CPT (1.71 ± 0.6 vs. 2.42 ± 0.7, P < 0.001) were lower in CSX patients than in controls. The differences between the two groups in CBF response to adenosine and in CBF response to CPT remained highly significant (P < 0.01 for both) after adjustment for all CVRFs, including serum CRP levels. Conclusion: In CSX patients, both endothelium-dependent and endothelium-independent CMVD cannot be reliably predicted by CVRFs (including serum CRP levels), alone or in combination