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Introduction: Coronary heart disease (CHD) is strongly associated with cognitive impairment, which is a core feature of depression, highly prevalent in patients with CHD. Interestingly, patients with CHD and individuals with depression display reduced heart rate variability (HRV), which proxies a complex network integrating autonomic and attentional systems. This study investigated the moderating role of depressive symptoms in the relation between reduced HRV and cognitive performance in patients with CHD., Method: The sample included 274 patients with CHD (mean [standard deviation] age = 62 [9.5] years; 13 % women) admitted to cardiac rehabilitation units. Visual attention and task switching were assessed through the Trail Making Test (TMT). Depressive symptoms were assessed with the Beck Depression Inventory-II (BDI-II). Resting electrocardiographic recordings were collected to compute HRV indices., Results: Patients with more severe depressive symptoms displayed an inverse association between HRV and cognitive performance (TMT-A: b = -0.08, p = .022; TMTB: b = -0.07, p = .042), whereas patients with milder depressive symptoms showed no significant association (TMT-A: b = -0.00, p = .90; TMTB: b = -0.02, p = .44)., Conclusions: Depressive symptoms may strengthen the relation between reduced HRV and poorer cognitive performance in cardiac patients. The presence of depressive symptoms may signal the dysfunction of a network subserving autonomic and cognitive function., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Objective: Poor vagally mediated heart rate variability (vmHRV) is a mechanism linking depression to coronary heart disease (CHD). Reduced vmHRV is also considered an index of emotion dysregulation-the frequent use of maladaptive emotion regulation strategies, one of the most important being expressive suppression-which is a key component of depression. Therefore, this study aimed to investigate the moderating role of expressive suppression in the relation between depression and vmHRV in patients with CHD., Methods: The sample included 235 patients with CHD (mean [standard deviation] age = 61.6 [9.8] years; 12% women) admitted to cardiac rehabilitation after a cardiac intervention. The Beck Depression Inventory-II was administered to assess depressive symptoms. Emotion regulation strategies based on either expressive suppression or cognitive reappraisal were assessed through the Emotion Regulation Questionnaire. Resting electrocardiographic recordings were collected for 5 minutes to compute HRV indices., Results: Expressive suppression moderated the relation between depressive symptoms and vmHRV ( b = -0.03, p = .012). Patients with lower expressive suppression scores showed no association between depressive symptoms and vmHRV ( b = -0.00, p = .94), whereas those with higher expressive suppression scores showed a significant negative association between depressive symptoms and vmHRV ( b = -0.05, p = .015)., Conclusions: The use of expressive suppression is likely to potentiate the relation between depressive symptoms and poor vmHRV, which could increase the cardiac risk in these patients. Targeting emotion regulation skills in cardiac rehabilitation programs may be useful for reducing the impact of depression in cardiac patients., (Copyright © 2022 by the American Psychosomatic Society.)

Mandatory quarantine during the COVID-19 pandemic had substantial negative consequences on psychological health in the general population. Depression, anxiety, and insomnia were reported to increase the morbidity and mortality risk in cardiac patients after cardiac interventions. Nonetheless, a gap in the evidence appeared regarding the effects of COVID-19-related quarantine on psychological outcomes in patients after cardiac interventions. The present study aimed to longitudinally investigate the effects of quarantine on depressive, anxiety, and insomnia symptoms in a group of patients who underwent cardiac intervention. Seventy-three patients admitted for cardiac rehabilitation completed a psychological assessment before and a reassessment after the quarantine and were included in the quarantine group. The control group included 76 patients who completed both evaluations before the quarantine. Depressive (Beck Depression Inventory-II; BDI-II), anxiety (Beck Anxiety Inventory-II; BAI), and insomnia (Sleep Condition Indicator; SCI) symptoms were evaluated in both groups at one (assessment) and eight (reassessment) months after cardiac intervention. The statistical analyses revealed that at reassessment, the quarantine group showed higher global depressive, anxiety, and insomnia symptoms than the control group and increased cognitive symptoms of depression. A higher presence of clinically relevant depressed patients was seen in the quarantine group. The present results showed that the COVID-19-related mandatory quarantine negatively affected psychological outcomes in patients after cardiac intervention, increasing the probability for these patients to be depressed. This, in turn, could influence patients' health in a critical period for morbidity and mortality risk. This underlines the priority of integrating and improving targeted mental health support as the pandemic continues, especially for cardiac patients., (© 2022. The Author(s).)

Aims: The exercise stress test is commonly used to assess physical capacity and recovery in coronary artery disease (CAD) patients after percutaneous transluminal coronary angioplasty (PTCA). Despite depressive symptoms have been consistently associated with adverse outcomes in CAD patients, they are rarely considered as risk factors of poor exercise test. The present study investigated the influence of depressive symptoms, along with anxiety, sleep problems and perceived health on exercise test in PTCA patients., Methods: One hundred and sixty-five patients who underwent PTCA completed the Beck Depression Inventory-II (BDI-II), the Beck Anxiety Inventory, the Sleep Condition Index and the 12-item Short-Form Health Survey and, after 20 days, underwent exercise stress test., Results: Higher BDI-II scores significantly predicted lower maximal workload measured in metabolic equivalents (METs; β = -0.13; p = .030), shorter total exercise duration (β = -5.23; p = .034) and the inability to reach maximum heart rate during exercise test (OR = 1.07; p = .032), even after controlling for relevant sociodemographic and biomedical risk factors., Conclusions: Depressive symptoms specifically predicted worse exercise stress test performance in patients after PTCA, controlling for common risk factors. Focusing on the assessment of depressive symptoms, in addition to sociodemographic and biomedical risk factors, is essential to anticipate patients at risk of poor physical capacity after PTCA., (Copyright © 2020. Published by Elsevier Inc.)

Annually, more than 100 million tourists are attracted by the mountainous areas around the world. On the one hand, leisure time activities at altitude may well contribute to the well-established beneficial effects of exercise; on the other hand, these activities are also associated with a relatively high risk of death. Sudden cardiac death (SCD) is the most frequent cause of nontraumatic death in males older than 34 years at altitude during leisure time activities such as downhill skiing and hiking. Whereas prior myocardial infarction is the most important risk factor for SCD, particularly relevant in downhill skiers, the unusual physical activity during the first days at altitude and the prolonged abstinence from food and fluid intake during exercise at altitude are the most important triggers. Unaccustomed physical activity seems more likely to trigger SCD than altitude per se. The detection of subjects at risk, evidence-based therapy, and advice on adequate behavior during the altitude sojourn will help to prevent SCD and to increase the health benefits generated by mountaineering activities.

Objective: Several previous studies evaluated the cardiovascular risk associated with exercise, but only a few papers considered this risk during physical activity in the mountains. The aim of this study was to assess the cardiovascular risk in a population practising physical activity in the mountains., Methods: We used an observational study design. We estimated the population by integrating the data of presences in the accommodation establishments with data from telephone and on-field interviews. As survey sources of cardiovascular events we used the reports of the Mountain Rescue teams and of the emergency physicians and pathologists operating in the hospitals of the considered mountain area., Results: We estimated that the duration of exposure to risk for the study population was, averagely per year, 12 449 877 person-days. During the study period, we recorded 117 cardiovascular events, namely 38 sudden cardiac deaths, 13 acute coronary syndromes, and five strokes. The remaining 61 events were non-traumatic events with a probable cardiovascular origin. We calculated one cardiovascular event per 319 000 person-days of physical activity in the mountains, one sudden cardiac death per 980 000 and one acute coronary syndrome per 2 895 000 person-days., Conclusions: The risk of cardiovascular events in the population practising physical activity in the mountains is very low and essentially limited to men over the age of 40, particularly if they do not practise regularly physical activity. For these subjects the risk seems to be associated with physical activity, but not with altitude and other typical aspects of mountains, such as low temperature and difficulties of terrain.

The annual incidence of stroke in patients with nonrheumatic atrial fibrillation averages 5% per year and increases with age, left ventricular dysfunction, hypertension, diabetes or prior stroke. Since in nonrheumatic atrial fibrillation 91% of left atrial thrombi are located in the left atrial appendage, in patients ineligible for oral anticoagulation it was suggested the percutaneous closure of left atrial appendage as a therapeutic option to reduce embolic risk. In this article we report our initial experience with this procedure, which was uneventful and efficacious at short-term follow-up. In conclusion, the interventional approach in patients with atrial fibrillation ineligible for oral anticoagulation seems feasible and promising, and deserves further investigation.

Purpose: The American Diabetes Association states that physical activity can be performed by individuals with Type 1 diabetes. Nevertheless, extreme altitude mountaineering represents a demanding challenge. We present the metabolic and cardiovascular parameters found in individuals with Type 1 diabetes during the ascent to Cho Oyu located at a height of 8201 m., Methods: Six individuals with Type 1 diabetes and 10 matched controls participated in the expedition. Both groups were evaluated before and after 4 h of trekking for vital indices, blood gases, acute mountain sickness, and metabolic control at 0, 3700, and 5800 m., Results: No difference between the groups was observed in acute mountain sickness scores. There was a progressive elevation in basal heart rates in both groups at increasing altitude while no changes were observed in mean blood pressures. After the 3 h of trekking, a significant increase in heart rate was observed in the controls at 0 m whereas a significant decrease in blood pressure was observed at higher altitude only in controls. HbA1c levels were worse after the expedition in both groups. A progressive increase in insulin requirement was observed in subjects with Type 1 diabetes (38 +/- 6 U x d(-1) at 0 m to 51 +/- 6 at 4200 m, P < 0.001). At an altitude of 5800 m, there was a significant increase in blood lactate concentration, independently of the activity level in the two groups., Conclusions: At extreme altitude, highly motivated trekkers with Type 1 diabetes but free from long-term complications present metabolic and cardiovascular parameters comparable with those of control subjects despite a worsening in metabolic control. This type of physical activity must be accompanied by careful glucose monitoring.

Italy is a mountainous country with a total of 88 huts and bivouacs at altitudes higher than 3,000 m. Starting in the 19th century a great deal of research in high altitude pathophysiology has been carried out in Italy and many Italian physicians have been involved in mountain medicine. Most of the Italian research has been carried out at two locations: the scientific laboratories "Angelo Mosso" on Monte Rosa (Capanna Regina Margherita and Laboratorio Angelo Mosso), and the "Pyramid" in Nepal. The Capanna Regina Margherita, located on the top of Punta Gnifetti (Monte Rosa, 4,559 m), was inaugurated in 1893. With the support of Queen Margherita of Savoy, an Observatory for scientific studies was built beside this hut in 1894. In 1980 the hut was completely rebuilt by the Italian Alpine Club. The Istituto Angelo Mosso at Col d'Olen, at the base of Monte Rosa (at 2,900 m) was inaugurated in 1907. The high altitude laboratory named the "Pyramid" was built in 1990. Made of glass and aluminium, this pyramid-shaped structure is situated in Nepal at 5,050 m. The scientific laboratories "Angelo Mosso" on Monte Rosa (mainly the Capanna Regina Margherita) and the Pyramid form a nucleus for high altitude research: the former is especially devoted to research regarding acute mountain sickness and the response to subacute hypoxia, whereas the latter is a unique facility for research responses to chronic hypoxia, the effect of exposure to very high altitude, and the study of the resident population living in the Himalayas for at least 25,000 years.

Even today, a restrictive attitude frequently leads the physician to discourage the patient with cardiovascular abnormalities from sojourning at an altitude over 1000 m. This attitude, however, is not supported by any scientific proof. After a review of the major cardiovascular adaptations during high altitude exposure, we reported the principal studies of the effects of high altitude on patients with coronary heart disease, particularly during exercise. On the basis of personal experience and of other authors, we can state that the patient with ischemic heart disease, asymptomatic and with a recent clinical and functional evaluation, can stay in the mountains, even at altitudes of 2000-3000 m, and can hike and ski (cross-country and downhill). The risks appear to be related to factors independent of altitude, such as excessive cold or intense emotional stress due to dangerous situations, conditions that must consequently be avoided. On the other hand, an individual approach should be followed for the other congenital and acquired heart diseases, in which case we must consider, in addition to the clinical situation, some peculiar aspects of mountain environment (hypoxia, isolation, difficult access to medical facilities). Finally, the hypertensive patient, expected to have higher blood pressure values, especially diastolic, should frequently record his values during the first week at high altitude, eventually adjusting the therapy.

During chronic high-altitude (HA) exposure, basal and exercise-induced noradrenaline (NA) increases do not parallel blood pressure (BP) changes observed; unlike beta-adrenergic receptors, to our knowledge no data are available on alpha-receptors. We studied platelet alpha 2- and leucocyte beta-receptors and basal catecholamine levels in 11 trained climbers before and after they had spent a 15-day period at a height of over 4400 m. In six of the climbers we also evaluated catecholamines after maximal bicycle ergometer exercise. After chronic high-altitude exposure, a significant decrease was found in platelet alpha 2-receptor density and affinity [Bmax from 92.6 +/- 6.7 to 54.6 +/- 4.2 fmol mg-1 protein (P < 0.001) and KD from 1.271 +/- 0.034 to 1.724 +/- 0.077 nmol L-1 (P < 0.05)], although no changes to beta-receptors were observed. No changes were found in basal pre- and post-expedition NA and adrenaline (A), and there was only a slight decrease in post-expedition NA after maximal exercise. Our results suggest that prolonged exposure to hypoxia induces a down-regulation of alpha 2-receptors, which may be a contributory factor in the regulation of the physiological vascular response to acclimatization.

Eight young healthy male subjects, members of a Himalayan expedition, underwent 24 h Holter monitoring before departure, after 1 and 4 weeks at high altitude (5000 m) and after return to sea level. At high altitude, the circadian reciprocal changes in low and high frequency (LF, HF) were absent, with no significant reduction in the LF to HF ratio over the 24 h; moreover, the proportion of adjacent R-R intervals that differed by more than 50 ms (pNN50) decreased significantly and remained lower after return to sea level. Urine catecholamines increased at high altitude, but only norepinephrine, after 1 week of exposure, rose significantly. Upon return to sea level the density, but not the affinity, of [alpha]2-adrenergic receptors on platelets decreased significantly compared to pre-expedition values. At high altitude increased sympathetic activity was indicated by elevation of urine norepinephrine and by the loss of circadian rhythm in spectral components. The simultaneous reduction of HF and pNN50 demonstrated decreased vagal tone. The persistence of increased sympathetic activity could explain the downregulation of adrenergic receptors after prolonged high altitude exposure.

Echocardiographic and Doppler studies were performed in 134 patients with a Hancock bioprosthesis in the mitral valve position during a follow-up period of 1 to 216 months. Among the xenografts, 57% were clinically normal and 43% had severe dysfunction. Among the normal bioprostheses, 35% had echocardiographically thickened mitral cusps (> or = 3 mm) with normal hemodynamic function; by setting the lower 95% confidence limit of valve area at 1.7 cm2 these patients had a significantly (p < 0.01) smaller valve area than that of normal control subjects. Evaluation of all thickened normal mitral valves showed the highest incidence of thickening at 9 years after implantation. Valve replacement surgery was subsequently performed in 33 patients with dysfunctioning bioprosthetic and echocardiographic diagnosis was confirmed in 91% of explanted valves (bioprosthetic stenosis 21%, incompetence 46%, and combined stenosis and regurgitation 33%). In 2 valves that were found to be stenotic on echocardiographic examination, a calcium-related commissural tear was also observed at reoperation, and in another, a paravalvular leak was found. Dystrophic calcification, isolated (64%) or occasionally associated with fibrous tissue overgrowth (21%), was the main cause of failure. Pannus was present in prostheses with longer satisfactory function (168 +/- 31 vs 124 +/- 21 months; p < 0.001). Long-term performance was evaluated by the Kaplan-Meier method for up to 18 years of follow-up. Freedom from structural valvular disfunction after mitral replacement was 89% at 6 years, 77% at 8 years, 56% at 10 years, 31% at 12 years, 16% at 15 years, and 15% at 18 years.

Left ventricular function after acute myocardial infarction depends on several mechanisms leading to left ventricular remodeling: (a) infarct size and healing and (b) adaptive changes involving both the dysfunctioning but viable myocardium (hibernating and stunned myocardium) and the nonischemic myocardium. The prognosis after acute myocardial infarction is strongly related to regional and global left ventricular function and the loss of dysfunctioning viable myocardium is a main factor in the worsening in left ventricular function in survivors of the acute phase. Thus, medical strategies should exert their beneficial effect on the "mechanical instability" of ventricular myocardium by saving the viable myocardium. beta-Blocker therapy has been shown to be effective in improving the prognosis via anti-ischemic and antiarrhythmic actions. The combination of metoprolol and nisoldipine seems to be able to preserve the contractile function of viable myocardium in the first 6 months after acute myocardial infarction.

The concept of myocardial stunning encompasses a wide variety of settings with major pathophysiological differences. Stresses, such as exercise-provoked myocardial ischaemia and dysfunction, are accompanied in most patients by a flow-limiting coronary stenosis, while contractile dysfunction persists in some with cessation of exercise. Twenty-six patients with proven coronary artery disease were studied by exercise echocardiography. Left ventricular (LV) volumes, wall motion and myocardial thickening were detected in apical four- and two-chamber views at rest and during upright bicycle exercise. All patients had an increase in total asynergy score and a decrease in ejection fraction (EF) during exercise. Myocardial dysfunction persisted after exercise in 22 patients (84%) as shown by the persistence of low values of LVEF on recovery up to 30 min. When compared to control, nisoldipine reduces total asynergy score and prevents the decline in LVEF during exercise by reducing the extent of myocardial ischaemia. The value of LVEF on recovery is normal. Thus, this particular form of myocardial stunning after exercise-induced ischaemia offers an interesting model for studying (1) the susceptibility of an individual patient and (2) to test the capability of a drug to prevent and to reverse myocardial stunning.

To analyse the role of changes in structure and function of the left ventricle in determining cardiac function at rest and during exercise, several two-dimensional and Doppler echocardiographic measurements were performed on 11 healthy subjects immediately before an Himalayan expedition (Nun, 7135 m), during acclimatization (3 weeks) and 14 days after the return. At rest decreases were found in cardiac index (CI) (3.23 l.min-1.m-2, SD 0.4 vs 3.82 l.min-1.m-2, SD 0.58, P less than 0.01), left ventricular mass (55.3 g.m-2, SD 9.4 vs 65.2 g.m-2, SD 13.5, P less than 0.005) and left ventricular end-diastolic volume (LVEDV) (53.9 ml.m-2, SD 6.9 vs 64.8 ml.m-2, SD 9.1, P less than 0.001) after acclimatization; by contrast the coefficient of peak arterial pressure to left ventricular end-systolic volume (PAP/ESV) (7.8, SD 1.6 vs 6.0, SD 1.8, P less than 0.005) and mean wall stress [286 kdyn.cm-2, SD 31 vs 250 kdyn.cm-2, SD 21 (2.86 N.cm-2, SD 0.31 vs 2.50 N.cm-2, SD 0.21), P less than 0.005] increased. After return to sea level, low values of CI and mass persisted despite a return to normal of LVEDV and preload. A reduction of PAP/ESV was also observed. At peak exercise, PAP/ESV (8.7, SD 2.4 vs 12.8, SD 2.0, P less than 0.0025), CI (9.8 l.min-1.m-2, SD 2.5 vs 11.6 l.min-1.m-2, SD 1.6, P less than 0.05) and the ejection fraction (69%, SD 6 vs 76%, SD 4, P less than 0.05) were lower after return to sea level than before departure.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasodilating agents acutely reduce regurgitant volume and improve left ventricular performance in aortic regurgitation, but more information is necessary about their long-term efficacy. To evaluate the effects of 12 months of therapy with nifedipine, a randomized, double-blind, placebo-controlled trial was performed in 72 asymptomatic patients with severe aortic regurgitation. At 12 months, patients receiving nifedipine had a significant reduction in left ventricular end-diastolic volume index (110 +/- 19 versus 136 +/- 22 ml/m2, p less than 0.01) and mass (115 +/- 19 versus 142 +/- 16 g/m2, p less than 0.01) measured by two-dimensional echocardiography. They also had a reduction in left ventricular mean wall stress (360 +/- 27 versus 479 +/- 36 kdyne/cm2, p less than 0.001) and an increase in ejection fraction (72 +/- 8% versus 60 +/- 6%, p less than 0.05). These data show that the long-term unloading action of nifedipine is able to reverse left ventricular dilation and hypertrophy and suggest that such therapy has the potential to delay the need for valve replacement in asymptomatic patients.

The parameters of a maximal exercise stress test, without therapy, 30 to 186 days after myocardial infarction were related to cardiac death, recurrent nonfatal infarction, coronary artery by-pass surgery, development of angina pectoris and ST segment depression during subsequent stress test in 209 patients. During a follow-up period of 9.5 to 119 months (medium 52) 12 patients died, 14 developed recurrent nonfatal myocardial infarction, 4 were submitted to coronary surgery, respectively 53 and 69 patients presented angina and ST segment depression at the first test, 23 and 33 developed them subsequently. Among the exercise parameters only the systolic blood pressure less than 140 mmHg was predictive of future mortality. Angina and ST segment depression when present at the first stress test were significantly related between them and with low heart rate, low maximal systolic blood pressure and low work load, but not with cardiac mortality, reinfarction and by-pass surgery. Our results show a low predictive value of the late maximal exercise test after a myocardial infarction. Probably that depends on evolution of coronary disease, which does not provide long-term prognostic informations.