Open data for assessing habitats degree of conservation at plot level. An example dataset of forest structural attributes in Val d'Agri (Basilicata, Southern Italy).

Forests supply multiple ecosystem services and host a large proportion of the Earth's terrestrial biodiversity. In particular, they provide habitats for many taxonomic groups which can be threatened by forest unsustainable management practices. Type and intensity of forest management are widely recognized as the main drivers of structure and functions in forests ecosystems. However, to better understand the impacts and the benefits deriving from forest management, there is a big need to standardize procedures of field data collection and data analysis. Here, we provide a georeferenced dataset of vertical and horizontal structure of forest types belonging to 4 habitat types, sensu Council Directive 92/43/EEC. The dataset includes structural indicators commonly linked to old-growth forests in Europe, in particular the amount of standing and lying deadwood. We collected data on 32 plots (24 of 225 m2, and 8 of 100 m2, according to different forests type) during spring and summer of 2022, in Val d'Agri (Basilicata, Southern Italy). The dataset we provide follows the common national standard for field data collection in forest habitat types, published by ISPRA in 2016 with the aim to promote a greater homogeneity in assessment of habitat conservation status at Country and biogeographical level, as requested by the Habitats Directive.

Early reduction in plasma norepinephrine during beta-blocking therapy with metoprolol in chronic heart failure.

BACKGROUND: The possible role exerted by modulation of sympathetic outflow in the clinical effects of beta-blockade in chronic heart failure was tested during short- and long-term treatment. METHODS AND RESULTS: Oral metoprolol (30-150 mg/day) was added to conventional therapy in 14 patients with idiopathic dilated cardiomyopathy, left ventricular ejection fraction (LVEF) of <0.45, and New York Heart Association class II or III. Norepinephrine plasma levels, which are an index of sympathetic activation, decreased by 27.57 +/- 18.03% after 1 month (P < .005), but returned to pretreatment levels after 6 months. LVEF increased by 7.7 +/- 6.0 ejection fraction units after 6 months (P < .005 vs baseline and P < .05 vs 1 month). Long-term beta-blockade resulted in nonsignificant improvements in functional class, symptom score, and oxygen consumption at peak exercise. After 1 month, the reduction in plasma norepinephrine levels and the changes in LVEF were inversely correlated (P < .01). No other correlation emerged during short- or long-term treatment. CONCLUSION: In conclusion, the reduction in plasma norepinephrine levels during short-term beta-blockade was not proportional to the clinical benefits and may have been attributed to the direct inhibition of sympathetic outflow. The early reduction in circulating norepinephrine levels may decrease cardiac performance through withdrawal of sympathetic support when the favorable effects of beta-blockade have not had time to occur. The role that sympathetic modulation may exert in the long-term clinical benefits of metoprolol deserves further investigation.

Influence of beta-blockade with metoprolol on symptoms and functional capacity of patients with idiopathic dilated cardiomyopathy.

Long-term treatment with beta-adrenergic blocking drugs has been shown to induce clinical amelioration in patients with chronic heart failure. However, the efficacy of these agents has not been consistent, and the mechanisms of their beneficial effects remain to be established. The present study evaluated the influence of oral metoprolol on symptoms and exercise tolerance of patients with idiopathic dilated cardiomyopathy (3 women and 9 men, left ventricular ejection fraction < 0.45, NYHA functional class II or III). One patient did not tolerate metoprolol, whereas 11 patients terminated the study. After 6 months of beta-blocking therapy, detectable improvements of symptoms (NYHA class and questionnaire-derived symptom score) were observed in 6 patients. Six patients reported an increase in functional capacity [oxygen consumption at peak exercise (VO2p) during cardiopulmonary exercise test]. For the whole group, no significant changes in symptoms and exercise tolerance were detected. During exercise, oxygen pulse (VO2/heart rate) and VO2/RPP (VO2/heart rate/systolic pressure) were significantly increased after 6 months on metoprolol (+35, 9% and +27.1%, respectively; both p < 0.01 vs baseline). In conclusion, beta-blocking therapy was well tolerated by the majority of patients, some of which reported improvement of symptoms and functional capacity. The observed increase on oxygen pulse and Vo2/RPP suggests that beta-blockade may reduce myocardial oxygen requirements in proportion to cardiac work. An increase in the energy available to myocardial cells for synthetic and reparative processes may thus account, at least in part, for the beneficial influence of long-term beta-blockade in heart failure patients.

Cardiovascular neural regulation during and after prolonged high altitude exposure.

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.

Silent ischemia and loss of reversible myocardial dysfunction following myocardial infarction.

Sixty-seven asymptomatic patients were enrolled after a first uncomplicated myocardial infarction (MI) so as to study the relevance of reversible myocardial dysfunction in determining left ventricular function soon after the acute episodes and 12 months later. Moreover, the potential role of silent ischemia in conditioning the evolutive aspects of contractile dysfunction has been investigated. Postextrasystolic potentiation during two-dimensional echocardiographic (2-D echo) monitoring has been used to detect the presence of viable myocardium in asynergic myocardial segments. Results of electrocardiographic (ECG) ambulatory monitoring at predischarge determined patient groups: Group A included 49 patients without ST changes during monitoring, while Group B included 18 patients with silent ischemia. Incidence of reversible myocardial dysfunction was similar in the two study groups (82 vs. 86%, p = NS). Group B patients were older (59.6 +/- 6.7 vs. 50.6 +/- 10.6 years, p < 0.015) and had lower ejection fractions (EFs, 43.4 +/- 6.4% vs. 51.2 +/- 8.3%, p = 0.026) and higher at-rest wall-motion scores (WMSs, 11.4 +/- 5.9 vs. 7.2 +/- 3.8, p = 0.019). Left ventricular end-diastolic volume (LVEDV) and potentiated WMS did not differ. At 1-year examination, Group B patients exhibited a greater LVEDV index (96 +/- 6.5 vs. 70.7 +/- 14 ml/m2, p < 0.002) with a worsening both in rest and in potentiated wall-motion score index (12.8 +/- 4.6 vs. 5.3 +/- 1.8, p < 0.001; 9.2 +/- 3.6 vs. 4.8 +/- 2.2, p < 0.001, respectively). Left ventricular EF remained significantly depressed in Group B patients (42 +/- 8.7% vs. 55.5 +/- 8.1%, p < 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise-induced left ventricular dysfunction in coronary heart disease. A model for studying the stunned myocardium in man.

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.

Changes in structure and function of the human left ventricle after acclimatization to high altitude.

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)

Monomorphic repetitive rhythms originating from the outflow tract in patients with minor forms of right ventricular cardiomyopathy.

We studied in detail 17 patients presenting with monomorphic repetitive ventricular rhythms having left bundle branch block morphology and right axis deviation. All had an apparently normal heart at physical examination. At chest radiography, three patients had mild cardiomegaly, and at electrocardiography, five patients had inverted T waves beyond V2. Five patients had syncope or near syncope. In seven patients the tachycardia occurred on effort. One patient died suddenly. The patients were extensively investigated, using cross-sectional echocardiography, complete haemodynamic and angiographic studies, electrophysiology and histology, to search for any structural basis of the arrhythmias. Tachycardia was sustained in 8 patients, nonsustained in 3, and consistent with accelerated idioventricular rhythm and repetitive paroxysmal ventricular tachycardia in 5 and 1 patients, respectively. Despite the differences in clinical and arrhythmologic features, similar abnormalities of right ventricular structure and/or wall motion were detected in all patients, consistent with localized forms of right ventricular cardiomyopathy. Different antiarrhythmic drugs were successfully used in twelve patients (the four patients with accelerated idioventricular rhythm were not treated). The patient who died suddenly had previously had a sustained ventricular tachycardia and was being treated by beta-blockade. Postmortem study revealed massive fibro-adipose substitution of the right ventricular free wall and pulmonary infundibulum.

[Prognostic value of late exercise test after myocardial infarction]. / Valore prognostico della prova da sforzo tardiva dopo infarto miocardico acuto.

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.

Relevance of subtle echocardiographic findings in the early diagnosis of the concealed form of right ventricular dysplasia.

Right ventricular dysplasia (RVD) is an important cause of arrhythmic sudden death in young people. Echocardiographic criteria suggestive of RVD were: dilation of RV, localized bulge and dyskinesia of the inferobasal wall, structural changes of the moderator band, isolated enlargement of RV outflow tract, apical dyskinesia and trabecular disarrangement. Among 136 subjects 'at risk of high incidence of RVD', 40 had a suggestive echocardiogram. 90% of these showed lipomatous transformation at biopsy and/or developed serious ventricular arrhythmias during a mean follow-up of 42 months. Thus, echocardiography is a potent method in detecting myocardial pathology due to RVD.

Contribution of cross-sectional echocardiography to the diagnosis of right ventricular dysplasia at the asymptomatic stage.

The value of cross-sectional echocardiography in the early diagnosis of right ventricular (RV) dysplasia in asymptomatic patients has been assessed. Criteria that defined RV dysfunction and structural abnormalities were developed from 38 normal subjects. Of 136 patients admitted into the study program, 40 (29.4%) had an echocardiogram suggestive of RV dysplasia using the following criteria: mild dilatation of the right ventricle (normal range defined as the 95% confidence limit of the values in the control group); localized bulge and dyskinesia of the infero-basal wall; structural changes of the moderator band; isolated enlargement of RV outflow tract; apical dyskinesia and trabecular disarrangement. Holter monitoring and a maximal exercise stress test at entry into the study and during the follow-up (mean 42, range 18-82 months) demonstrated serious ventricular arrhythmias, and RV endomyocardial biopsy confirmed the diagnosis of RV dysplasia in most of these patients, characterized by an electrical instability of RV myocardium (82.5%). During the follow-up, a marked enlargement of RV cavity appeared in three other patients, and RV endomyocardial biopsy demonstrated the typical findings in all patients.

Juvenile sudden death and effort ventricular tachycardias in a family with right ventricular cardiomyopathy.

A family with occurrence of juvenile sudden death and effort polymorphous ventricular tachycardias is reported. Nineteen members aged 9 to 63 years were investigated. Four of them died suddenly in their youth. Postmortem investigation performed in 2 deceased subjects disclosed an apparently normal heart at macroscopy but fibro-fatty substitution of the right ventricular free wall was noted at histologic examination. The 14 living members underwent physical examination, resting electrocardiography, chest X-radiography, Holter monitoring, exercise stress testing, and M-mode and cross-sectional echocardiography. Four patients underwent hemodynamic and electrophysiologic studies. All 14 subjects had normal physical examination as well as normal electrocardiographic and cardiothoracic indices. Localized right ventricular structural and dynamic abnormalities were noted at cross-sectional echocardiographic and angiographic investigation of 9 of the patients. The right ventricular volumes in these subjects were normal or slightly increased. In 7 of them, polymorphous ventricular tachycardias were induced by exercise stress testing. The arrhythmias which were responsive to beta-blockade, do not seem to depend on reentry. Enhanced automaticity appeared to be the more likely mechanism of their production. These data demonstrate that right ventricular cardiomyopathy may occur in an occult form with life-threatening electrical instability.

[Type A personality and risk of post-infarction coronary events]. / Personalità di tipo A e rischio di eventi coronarici nel post-infarto.

The purpose of this study was to verify the prevalence of Coronary-prone Behaviour Pattern in a group of eighty-eight patients recovering from their first episode of myocardial infarction. These patients were followed for a period of 4 years to verify the eventual appearance of coronary events, after their first myocardial infarction, with high Coronary-prone Behaviour Pattern levels. The results showed that the number of subjects who died from recurrent myocardial infarction was nearly twice as high in type B, non coronary-prone subjects, as in type A subjects. The Authors hypothesize that specific ways of coping with stressful events adopted by type A subjects may constitute a protection factor as regards the risk of death from recurrent myocardial infarction.

Low- and medium-dose diltiazem in chronic atrial fibrillation: comparison with digoxin and correlation with drug plasma levels.

The safety and efficacy of diltiazem were compared with digoxin maintenance therapy for control of ventricular response in 19 patients with chronic atrial fibrillation. The relationship between drug plasma levels and cardiovascular effects was also investigated. After 7 days of combined therapy with diltiazem (60 mg three times a day in 10 patients and four times a day in nine patients) and digoxin (0.125 mg/day in two patients and 0.250 mg/day in 17 patients), the 24-hour mean heart rate derived from ambulatory ECG recording was reduced by 16.3% in comparison with digoxin therapy alone; the serum digoxin level was not significantly changed (1.06 +/- 0.43 vs 1.05 +/- 0.61 ng/ml). After a standardized bicycle exercise test (50 watts for 3 minutes), maximal heart rate was reduced by 19.9%, diastolic blood pressure was decreased by 8.9%, and systolic pressure-rate product was decreased by 12.5%. Diltiazem plasma levels (mean 120.9 +/- 63.3 ng/ml) were linearly correlated with percentage variations in maximal heart rate, diastolic blood pressure, systolic blood pressure, and pressure-rate product during exercise. Eighteen patients in succession discontinued digoxin therapy; after 14 days of diltiazem alone, the 24-hour mean heart rate returned to control values of digoxin therapy, whereas maximal heart rate and pressure-rate product during exercise were significantly reduced (-17.2% and -14.1%, respectively), with no changes in blood pressure. Diltiazem plasma levels (135.0 +/- 83.2 ng/ml) showed a linear correlation with the percentage of reduction in maximal heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia.

Five apparently healthy people (aged 16-47) presented with recurrent episodes of accelerated idioventricular rhythm characterised by left bundle branch block and right axis deviation. Clinical history, physical findings, basic electrocardiogram, chest x ray, and blood tests were within normal limits in all. Holter monitoring, exercise stress test, and electrophysiological study (in three patients) showed that accelerated idioventricular rhythm was mainly bradycardia dependent, easily suppressed by effort and overdrive pacing, and originated from the outflow tract of the right ventricle. The mechanism could be enhanced automaticity. Data from cross sectional echocardiography (in all patients) and from haemodynamic evaluation (in three) identified structural or wall motion abnormalities of the right ventricle or both without appreciable dilatation of the ventricle. Biopsy specimens of the right ventricular endomyocardium showed fibrosis in one patient, fibrosis and fatty infiltration in the second, and pronounced fatty infiltration in the third. These results show that some patients with accelerated idioventricular rhythm have right ventricular abnormalities that are typical of the localised and concealed forms of arrhythmogenic right ventricular dysplasia.

[Arrhythmogenic right ventricular dysplasia. Study of a selected population]. / La displasia aritmogena del ventricolo destro. Studio su una popolazione selezionata.

268 patients (pts) aged between 4 and 63 (average block 33.6) years were examined in an effort to detect structural and/or wall motion abnormalities of the right ventricle, consistent with a diagnosis of Arrhythmogenic Right Ventricular Dysplasia (ARVD). The patients included in this study had some of these features: 1) sudden juvenile death (age less than 35 years) due to heart disease; 2) relatives of pts died suddenly of pathologically proven ARVD; 3) pts with ventricular arrhythmias grade Lown greater than 3, and with QRS morphology mainly of left bundle branch block; 4) pts between the ages of 18 and 40, with negative T waves beyond V2; 5) pts with ventricular arrhythmias of left bundle branch block morphology, and grade Lown greater than 1, and negative T waves beyond V1. ARVD was recognized in 108 living and 18 deceased pts. Our data confirm that ARVD is a wide spectrum disease, going from the classical form described by Marcus and Fontaine to concealed forms characterized mainly by premature ventricular complexes.

Sensitivity, specificity and predictive accuracy of Q wave, QX/QT ratio, QTc interval and ST depression during exercise testing in men with coronary artery disease.

One hundred forty-three subjects (107 with coronary artery disease [CAD], 23 without CAD [evaluated by coronary angiography] and 13 athletes) were selected for this study. All subjects underwent exercise testing to evaluate sensitivity, specificity and predictive value of Q wave, QX/QT ratio, QTc interval and ST depression. The Q-wave analysis revealed less sensitivity (49%) and less specificity (83%) than ST depression (71% and 97%, respectively). The QTc criterion had greater sensitivity (80%) than ST depression but less specificity (11%). The QX/QT criterion was no different in sensitivity (74%) but had less specificity (69%). To establish the statistical evaluation of the positive predictive value in CAD, variations in the prevalence of the disease were considered. A 90% prevalence gives the best positive predictive value on all evaluated measurements, between 100% for ST depression and 89% for the QTc criterion. A 5% prevalence, however, gives an acceptable positive predictive value only on ST-segment depression (57%).