Comparison of Perioperative and Postoperative Outcomes Among 3 Left Atrial Incisions: Conventional Direct, Transseptal, and Superior Septal Left Atriotomy.

BACKGROUND: Achieving optimal exposure of the mitral valve during surgical intervention poses a significant challenge. This study aimed to compare perioperative and postoperative outcomes associated with 3 left atriotomy techniques in mitral valve surgery-the conventional direct, transseptal, and superior septal approaches-and assess differences during the surgical procedure and the postoperative period. METHODS: Inclusion criteria were patients undergoing mitral valve surgery from January 2010 to December 2020, categorized into 3 cohorts: group 1 (conventional direct; n = 115), group 2 (transseptal; n = 33), and group 3 (superior septal; n = 59). To bolster sample size, the study included patients undergoing mitral valve surgery independently or in conjunction with other procedures (eg, coronary artery bypass grafting, aortictricuspid surgery, or maze procedure). RESULTS: No substantial variance was observed in the etiology of mitral valve disease across groups, except for a higher incidence of endocarditis in group 3 (P = .01). Group 1 exhibited a higher frequency of elective surgeries and isolated mitral valve procedures (P = .008), along with reduced aortic clamping and cardiopulmonary bypass durations (P = .002). Conversely, group 3 patients represented a greater proportion of emergency procedures (P = .01) and prolonged intensive care unit and hospital stays (P = .001). No significant disparities were detected in terms of permanent pacemaker implantation, postoperative complications, or mortality among the groups. CONCLUSION: Mitral valve operations that employed these 3 atriotomy techniques demonstrated a safe profile. The conventional direct approach notably reduced aortic clamping and cardiopulmonary bypass durations. The superior septal method was primarily employed for acute pathologies, with no significant escalation in postoperative arrhythmias or permanent pacemaker implantation, although these patients had prolonged intensive care unit and hospital stays. These outcomes may be linked to the underlying pathology and nature of the surgical intervention rather than the incision method itself.

L-NAME iontophoresis: a tool to assess NO-mediated vasoreactivity during thermal hyperemic vasodilation in humans.

BACKGROUND: Decreased endothelial Nitric oxide (NO) bioavailability is one of the earliest events of endothelial dysfunction. Assessment of microvascular blood flow using a Laser Doppler Imager during local noninvasive administration of L-N-Arginine-Methyl-Ester (L-NAME) by skin iontophoresis may help discriminate the relative contributions of NO and non-NO pathways during a skin thermal hyperemic test. METHODS: In healthy nonsmokers, the effects of thermal vasodilation and sodium nitroprusside-mediated vasodilation were tested on skin pretreated with 0.9% saline solution, 2% L-NAME iontophoresis (n = 12), or intradermal injection of 25 nmol L-NAME (n = 10). The effects of L-NAME iontophoresis were also measured in a group of smokers (n = 10). RESULTS: L-NAME iontophoresis and intradermal injection of L-NAME decreased the skin response to local heating to a similar degree (-41% ± 4% vs. -44% ± 6%). L-NAME iontophoresis site-to-site and day-to-day coefficients of correlation were 0.83 and 0.76, respectively (P < 0.01). The site-to-site and day-to-day coefficients of correlation of L-NAME injection were lower than those of iontophoresis at 0.66 (P < 0.05) and 0.12, respectively (P = not significant). Sodium nitroprusside-induced skin hyperemia was not affected by L-NAME administration. L-NAME iontophoresis-mediated inhibition of skin thermal hyperemia was greater in smokers than in nonsmokers (P < 0.05). CONCLUSIONS: Laser Doppler Imager assessment of skin thermal hyperemia after L-NAME iontophoresis provides a reproducible and selective bedside method of qualitatively analyzing the contribution of the NO pathway to microvascular vasomotor function.

Acute effects of nicotine on arterial stiffness and wave reflection in healthy young non-smokers.

1. Recently, we have demonstrated that cigarette smoke exposure proportionally increases plasma nicotine levels and arterial wave reflection to the aorta. However, the exact contribution of nicotine to the smoke-induced enhancement of wave reflection and the potential underlying mechanisms have not been fully investigated. 2. The present study was a prospective study in 15 healthy male non-smokers. All received a placebo and a 2 mg nicotine tablet, according to a randomized double-blind cross-over study design. Each subject underwent repeated measurements at baseline and for 1 h after nicotine or placebo intake, using carotid-femoral pulse wave velocity (PWV) to assess arterial compliance. Concurrently, aortic pressures and the augmentation index were evaluated using applanation tonometry. 3. Plasma nicotine concentrations achieved 1 h after intake of the nicotine tablet reached comparable levels to those achieved after 1 h exposure to passive smoke (3.6 +/- 0.4 vs 3.2 +/- 0.4 ng/mL, respectively; P = 0.4). 4. Nicotine enhanced arterial wave reflection to the aorta, as assessed by the augmentation index corrected for heart rate (4.2 +/- 1.3 vs-0.7 +/- 0.8% with placebo; P = 0.001). In addition, a progressive increase in carotid-femoral PWV was noted after nicotine administration (0.3 +/- 0.1 vs-0.02 +/- 0.1 m/s with placebo; P = 0.04). This remained significant even after adjustment for changes in mean blood pressure and heart rate (P = 0.01). 5. Plasma nicotine concentrations comparable to those achieved after exposure to passive smoke enhance arterial wave reflection to the aorta. This is accompanied by an increase in carotid-femoral PWV, denoting a deterioration of arterial compliance by nicotine.

Acute effects of passive smoking on peripheral vascular function.

Environmental tobacco smoke (ETS) acutely affects peripheral and coronary vascular tone. Whether ETS exerts specific deleterious effects on aortic wave reflection through nicotine exposure, whether they persist after ETS cessation, and whether the smoke environment impairs microvascular function and increases asymmetrical dimethyl-arginine levels are not known. We tested these hypotheses in a randomized, crossover study design in 11 healthy male nonsmokers. The effects of 1 hour of exposure to ETS, as compared with a nontobacco smoke and normal air, on augmentation index corrected for heart rate and skin microvascular hyperemia to local heating were examined. Augmentation index increased both during (P=0.01) and after (P<0.01) the ETS session but remained unchanged in the nontobacco smoke session when compared with normal air. Nicotine levels after the exposure were related to the peak rise in augmentation index (r=0.84; P<0.01), denoting a predominant role of nicotine in ETS vascular effects. This was confirmed in a second set of experiments (n=14), where the sublingual administration of nicotine was associated with an acute impairment in wave reflection as compared with placebo (P=0.001). Both ETS and nontobacco smokes increased plasma asymmetrical dimethyl-arginine levels (P<0.001), but only ETS reduced the late rise in skin blood flow in response to heating (P=0.03). In conclusion, passive smoking specifically increases aortic wave reflection through a nicotine-dependent pathway and impairs microvascular function, even after the end of the exposure. However, both tobacco and nontobacco passive smoking inhalation increase plasma asymmetrical dimethyl-arginine levels.

Beneficial effect of angiotensin II type 1 receptor blocker antihypertensive treatment on arterial stiffness: the role of smoking.

The purpose of the present study was to assess angiotensin receptor blocker (ARB) treatment on arterial stiffness in select hypertensive patients and define possible differences between smokers and nonsmokers. The authors evaluated 81 consecutive, nondiabetic patients (mean age, 52 years; 47 men) with uncomplicated essential hypertension with high plasma renin activity who were administered monotherapy with irbesartan, an ARB, at maximal dose. Patients were divided into smokers (n=24) and nonsmokers (n=57). Carotid-radial pulse wave velocity (PWVc-r), carotid-femoral pulse wave velocity (PWVc-f), and augmentation index (AIx) were measured before and 6 months after ARB antihypertensive treatment. All mean values of elastic effect indices were decreased after irbesartan monotherapy (AIx, from 26.3%to 21.2% [P<.01;] PWVc-f, from 7.7 m/s to 7.3 m/s [P<.05], and PWVc-r, from 8.9 m/s to 8.3 m/s [P<.001]). When comparing smokers vs nonsmokers, no difference was noted in AIx and PWVc-f change (P=not significant), while PWVc-r change was greater in smokers compared with nonsmokers (P<.05). Chronic ARB treatment may favorably affect arterial stiffness and wave reflections in hypertensive chronic smokers with elevated plasma renin levels.

New insights into the sympathetic, endothelial and coronary effects of nicotine.

1. Nicotine is a well studied pleiotropic agent which occurs naturally in tobacco smoke and has been largely accused for many of the adverse effects of smoking on the cardiovascular system, including autonomic imbalance, endothelial dysfunction and coronary blood flow dysregulation. 2. The acute sympathoexcitatory effects of smoking on the cardiovascular system are partially mediated by catecholamine release, muscle sympathetic nerve excitation and peripheral chemoreceptor sensitivity increase, consecutive to nicotinic receptor stimulation in the autonomic nervous system. 3. Recent animal data suggest that nicotine promotes the oxidative and inflammatory stress to the endothelium and induces pathological angiogenesis, leading to the progression of the atherosclerotic lesions. 4. Nicotine increases myocardial work without impairing the physiological coronary vasodilatation. Consequently, nicotine per se cannot explain the sudden reduction in coronary flow reserve after exposure to both active and passive smoking. 5. Nicotine's biological effects are characterized by a rapid onset of tolerance, which can explain why nicotine administration does not elicit acute coronary and chemoreflex side-effect in smokers.

Nicotine increases chemoreflex sensitivity to hypoxia in non-smokers.

BACKGROUND: The peripheral chemoreflex contributes to cardiovascular regulation and represents the first line of defence against hypoxia. The effects of nicotine on chemoreflex regulation in non-smoking humans are unknown. METHOD: We conducted a prospective, randomized, crossover, and placebo-controlled study in 20 male non-smokers to test the hypothesis that nicotine increases chemoreflex sensitivity. The effects of two intakes of 2 mg nicotine tabs and placebo on sympathetic nerve activity to muscle circulation (muscle sympathetic nerve activity; MSNA), minute ventilation (Ve), blood pressure and heart rate were assessed during normoxia, moderate isocapnic hypoxia, hyperoxic hypercapnia and an isometric handgrip in 10 subjects. Maximal end-expiratory apnoeas were performed at baseline and at the end of the fifth minute of hypoxia. In a second experimental setting, we studied the ventilatory response to a more marked isocapnic hypoxia in 10 other volunteers. RESULTS: Mean MSNA and Ve were not modified by nicotine during the 5 min of normoxia or moderate hypoxia. In the presence of nicotine MSNA was related to oxygen desaturation (P < 0.01). The sympathoexcitatory effects of nicotine became especially evident when apnoeas achieved oxygen saturations less than 85% (511 +/- 44% increase in MSNA after the first intake, and 436 +/- 43% increase after the second intake versus 387 +/- 56% and 338 +/- 31% with placebo, respectively, P < 0.05). Nicotine also increased the ventilatory response compared with placebo when oxygen saturation decreased to less than 85% (P < 0.05). CONCLUSION: This is the first study to demonstrate that nicotine increases peripheral chemoreflex sensitivity to large reductions in arterial oxygen content in healthy non-smokers.

Beneficial effects of angiotensin II type 1 receptor blocker antihypertensive treatment on inflammation indices: the effect of smoking.

The effect of long-term angiotensin II type 1 receptor blocker (ARB) therapy on inflammation indices has not been fully investigated in a hypertensive population. The authors evaluated 323 consecutive nondiabetic patients (mean age, 57 years; 176 men; 92 smokers) with high renin activity and uncomplicated essential hypertension whose blood pressure levels normalized (from 163.9/100.7 mm Hg to 131.6/82.8 mm Hg) after 4 weeks of ARB or ARB/diuretic treatment. All patients underwent full laboratory evaluation (routine examination of blood and urine, liver, kidney, thyroid function, and lipid and glucose profiles), including measurement of high-sensitivity C-reactive protein and serum amyloid A levels, at drug-free baseline, which was repeated after 6 months of ARB or ARB/diuretic treatment. A significant (P<.001) overall decrease was noted in both high-sensitivity C-reactive protein (-0.41+/-1.56 mg/dL) and serum amyloid A (-0.62+/-2.03 mg/dL), but a smaller decrease in high-sensitivity C-reactive protein and serum amyloid A change was seen in the smoker subgroup compared with nonsmokers (P<.05), indicating that the ARB or ARB/diuretic anti-inflammatory effect may be adversely affected by smoking status.