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BACKGROUND In advanced heart failure (HF), Levosimendan increases peak oxygen uptake (peakVO2). We investigated whether peakVO2 increase is linked to cardiovascular, respiratory or muscular performance changes. METHODS AND RESULTS Twenty patients hospitalized for advanced HF underwent, before and shortly after Levosimendan infusion, two different cardiopulmonary exercise tests (CPET): a) a personalized ramp protocol with repeated arterial blood gas analysis and standard spirometry including alveolar-capillary gas diffusion measurements at rest and at peak exercise, and b) a step incremental workload CPET with continuous near-infrared spectroscopy analysis and cardiac output (CO) assessment by bioelectrical impedance analysis. Levosimendan significantly reduced natriuretic peptides, improved peakVO2 (11.3 [IQR 10.1-12.8] to 12.6 [10.2-14.4] ml/Kg/min, p

Background: The role of risk scores in heart failure (HF) management has been highlighted by international guidelines. In contrast with HF, which is intrinsically a dynamic and unstable syndrome, all its prognostic studies have been based on a single evaluation. We investigated whether time-related changes of a well-recognized risk score, the MECKI score, added prognostic value. MECKI score is based on peak VO2, VE/VCO2 slope, Na+, LVEF, MDRD and Hb. Methods: A multi-centre retrospective study was conducted involving 660 patients who performed MECKI re-evaluation at least 6 months apart. Based on the difference between II and I evaluation of MECKI values (MECKI II - MECKI I = ∆ MECKI) the study population was divided in 2 groups: those presenting a score reduction (∆ MECKI 0, clinical deterioration). Results: The prognostic value of MECKI score is confirmed also when re-assessed during follow-up. The group with improved MECKI (366 patients) showed a better prognosis compared to patients with worsened MECKI (294 patients) (p < 0.0001). At 1st evaluation, the two groups differentiated by LVEF, VE/VCO2 slope and blood Na+ concentration, while at 2nd evaluation they differentiated in all 6 parameters considered in the score. The patients who improved MECKI score, improved in all components of the score but hemoglobin, while patients who worsened the score, worsened all parameters. Conclusions: This study shows that re-assessment of MECKI score identifies HF subjects at higher risk and that score improvement or deterioration regards several MECKI score generating parameters confirming the holistic background of HF.

To date, the pandemic spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has involved over 100 countries in a matter of weeks, and Italy suffers from almost 1/3 of the dead cases worldwide. In this report, we show the strategies adopted to face the emergency at Centro Cardiologico Monzino, a mono-specialist cardiology hospital sited in the region of Italy most affected by the pandemic, and specifically we describe how we have progressively modified in a few weeks the organization of our Heart Failure Unit in order to cope with the new COVID-19 outbreak. In fact, on the background of the pandemic, cardiovascular diseases still occur frequently in the general population, but we observed consistent reduction in hospital admissions for acute cardiovascular events and a dramatic increase of late presentation acute myocardial infarction. Despite a reduction of healthcare workers number, our ward has been rearranged in order to take care of both COVID-19 and cardiovascular patients. In particular according to a triple step procedure we divided admitted patients in confirmed, suspected and excluded cases (respectively allocated in “red”, “pink” and “green” separated areas). Due to the absence of definite guidelines, our aim was to describe our strategy in facing the current emergency, in order to reorganize our hospital in a dynamic and proactive manner. To quote the famous Italian writer Alessandro Manzoni ‘It is less bad to be agitated in doubt than to rest in error.’

Alveolar β2-receptor blockade worsens lung diffusion in heart failure (HF). This effect could be mitigated by stimulating alveolar β2-receptors. We investigated the safety and the effects of indacaterol on lung diffusion, lung mechanics, sleep respiratory behavior, cardiac rhythm, welfare, and exercise performance in HF patients treated with a selective (bisoprolol) or a non-selective (carvedilol) β-blocker. Study procedures were performed before and after indacaterol and placebo treatments according to a cross-over, randomized, double-blind protocol in forty-four patients (27 on bisoprolol and 17 on carvedilol). No differences between indacaterol and placebo were observed in the whole population except for a significantly higher VE/VCO2 slope and lower maximal PETCO2 during exercise with indacaterol, entirely due to the difference in the bisoprolol group (VE/VCO2 31.8 ± 5.9 vs. 28.5 ± 5.6, p ETCO2 36.7 ± 5.5 vs. 37.7 ± 5.8 mmHg, p

Funding Acknowledgements Type of funding sources: None. Background. Atrial fibrillation (AF) is the most common cardiac arrhythmia causing left atrial appendage thrombosis (LAA-T) which can result in cerebral and systemic embolism. Nowadays, both vitamin K antagonists (VKA) and Direct Oral Anti Coagulants (DOAC) are effective for the prevention of ischaemic stroke in AF. Transesophageal echocardiography (TEE) is the best method to detect LAA-T in AF. However, data on the prevalence of LAA-T are lacking. Purpose. The aim of the study was 1) to evaluate the prevalence of LAA-T in patients affected by AF, receiving different anticoagulation regimens and candidates to cardioversion or catheter ablation 2) to correlate the presence of LAA-T with clinical and echocardiographic data. Methods. This is an observational, single-center study including 796 patients (73% male) with AF. TEE before cardioversion or catheter ablation was performed in all patients. Patients with mechanical prosthetic valve and severe mitral stenosis were excluded. Patients were divided in 2 groups according to anticoagulation regimen: Group 1 including patients on DOAC (dabigatran, rivaroxaban, apixaban, edoxaban) and Group 2 including patients on VKA at therapeutic dose. Results Group 1 included 369 patients (46%), Group 2 427 (54%). Age, CHA2DS2-VASc score, sex and pathology distribution (lone FA, hypertension, valve disease, ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy) were similar in the 2 groups. The overall prevalence of LAA-T was 43 cases (5%). Similar percentage of LAA-T was found regardless of anticoagulation regimen (Group 1: 16 cases, 4%; Group 2: 27 cases, 6%, p = 0.220). No difference in LAA-T prevalence was detected within Group 1 for different DOACs (p = 0.547). Patients with LAA-T were more frequently older (p = 0.023), female (p = 0.001), with higher CHA2DS2-VASc score (p = 0.002), affected by hypertrophic cardiomyopathy (p = 0.019), valve disease or bioprostetic valve (p = 0.001) regardless of anticoagulation regimen. A total of 697 patients (88%) were scheduled for cardioversion or catheter ablation. Cardioversion was successful in 667 patients (95%) without any ischemic event. Only 1 patient (0.1%) undergoing catheter ablation had a major ischemic event. Conclusions Efficacy of anticoagulation with VKA and DOAC is similar in preventing LAA-T in patients with AF. However, despite optimal adherence to a therapeutic regimen, several clinical factors (age, gender, high CHA2DS2-VASc score, hypertrophic cardiomyopathy and valvular disease) were associated with higher prevalence of LAA-T. TEE guided approach to cardioversion may prevent the risk of embolic events regardless of anticoagulation regimen used.

Background Sacubitril/valsartan is a first-in-class angiotensin receptor-neprilysin inhibitor (ARNI) recommended in the guidelines to reduce morbidity and mortality in patients with symptomatic heart failure (HF) with reduced ejection fraction (HFrEF). Although the recent widespread use of the drug, data on left ventricle (LV) reverse remodeling and improvement in functional capacity (FC) under treatment are still lacking. Case presentation A 73 years old man with a known HFrEF was admitted to the hospital for clinical review due to progressive worsening dyspnea in the last 6 months (NYHA class III) with high NTproBNP values. Echocardiography showed dilated LV (EDVi/ESVi 137/98 ml/m2) with severe reduction in ejection fraction (EF), moderate/severe aortic incompetence, moderate functional mitral regurgitation. A maximal, ramp-protocol, cardiopulmonary exercise test (CPET) showed a moderate reduction in FC with signs of cardiogenic limitation. He was started on Sacubitril/Valsartan 24/26mg b.i.d. with progressive up-titration of the dose until a maximum dose of 97/103mg b.i.d. and without any other change in the therapy. ARNI was well tolerated without hypotension, worsening renal function or hyperkaliemia. After 3 months the echocardiography showed a reduction in LV volumes (EDVi/ESVi 112/72 ml/m2) with mild improvement in EF (from 28% to 34%) and increased FC, leading to a 56% reduction in estimated HF mortality at 2 years assessed through MECKI Score (See tab. 1 and Fig. 1). NTproBNP value was also reduced compared to baseline. Conclusion We present a case of a short term improvement in LV and atrium volumes and FC after 3 months of treatment with Sacubitril/valsartan in a patient with HFrEF. More studies are needed to assess LV volumes and CPET values response to ARNI. Tab.1 Basaline 3 months Δ NYHA Class II III - MECKI Score (%) 5.12 2.23 -56-4% Peak VO2 /% of predicted) 60 72 +20% Maximal Work (W) 68 83 +22.1% Mitral regurgitation ++ + - eGFR (ml/min/1,73m2) 64 65 +1.6% Potassium (mmol/L) 4.26 4.20 -1.4% Aortic regurgitation +++ ++ - Clinical changes after the 3 months follow-up Abstract P638 Figure. Fig. 1

Blood stasis is the main cause of left atrial thrombosis (LAT) in atrial tachyarrhythmias. The high-velocity flow inside the left atrium, due to mitral valve regurgitation, may prevent clot formation but the topic has never been investigated in large-scale studies. The aim of our study was to evaluate whether the presence and degree of mitral regurgitation have a protective role against LAT risk.A total of 1302 consecutive adult patients with paroxysmal or persistent atrial fibrillation or flutter undergoing cardioversion, submitted to transesophageal echocardiography, were retrospectively enrolled in the study. The study population was divided into three groups according to the mitral regurgitation degree: absent, mild-to-moderate and severe.Among 1302 patients enrolled in the study, patients without mitral regurgitation were 248 (19%), those with mild-to-moderate 970 (75%), whereas 84 had severe mitral regurgitation (6%). LAT incidence was significantly lower in patients with severe mitral regurgitation compared with those with mild-to-moderate (mitral regurgitation) (2.4 vs. 8.9%, P 0.05), and similar to subjects without mitral regurgitation (2.4%).Despite patients with severe regurgitation having clinical and echo characteristics predisposing to LAT (higher age, heart failure, higher atrial size, lower ventricular function) thrombosis prevalence was significantly lower than for those with mild-to-moderate mitral regurgitation. The percentage of LAT in severe mitral regurgitation cases was very low and similar to that of cases without regurgitation which were characterized by lower age, normal left ventricular function or other risk factors, reinforcing the hypothesis of a protecting role against atrial thrombosis of mitral regurgitation.

SUMMARY Aim: To assess the effect of chronotropic incompetence on functional capacity in chronic heart failure (CHF) patients, as evaluated as NYHA and peak oxygen consumption (pVO2), focusing on the presence and dose of β-blocker treatment. Methods: Nine hundred and sixty-seven consecutive CHF patients were evaluated, 328 of whom were discarded because they failed to meet the study criteria. Of the 639 analyzed, 90 were not treated with β-blockers whereas the other 549 were. The latter were further subdivided in high (n = 184) and low (n = 365) β-blockers daily dose group in accordance with an arbitrary cut-off of 25 mg for carvedilol and of 5 mg for bisoprolol. Failure to achieve 80% of the percentage of maximum age predicted peak heart rate (%Max PHR) or of HR reserve (%HRR) constituted chronotropic incompetence. Results: No differences were found in NYHA or pVO2 between patients with and without β-blockers and, similarly, between high and low β-blocker dose groups. Twenty and sixty-nine percent of not β-blocked patients showed chronotropic incompetence according to %Max PHR and %HRR, respectively, whereas this prevalence rose to 61% and 84% in those on β-blocker therapy. Patients taking β-blockers without chronotropic incompetence, as inferable from both %Max PHR and %HRR, showed higher NYHA and pVO2 regardless of drug dose, whereas, in not β-blocked patients, only %HRR revealed a difference in functional capacity. At multivariable analysis, HR increase during exercise (ΔHR) was the variable most strongly associated to pVO2 (β: 0.572; SE: 0.008; P < 0.0001) and NYHA class (β: −0.499; SE: 0.001; P < 0.0001). Conclusions: ΔHR is a powerful predictor of CHF severity regardless of the presence of β-blocker therapy and of β-blocker daily dose.

Background Large files produced by standard compression algorithms slow down spread of digital and tele-echocardiography. We validated echocardiographic video high-grade compression with the new Motion Pictures Expert Groups (MPEG)-4 algorithms with a multicenter study. Methods Seven expert cardiologists blindly scored (5-point scale) 165 uncompressed and compressed 2-dimensional and color Doppler video clips, based on combined diagnostic content and image quality (uncompressed files as references). One digital video and 3 MPEG-4 algorithms (WM9, MV2, and DivX) were used, the latter at 3 compression levels (0%, 35%, and 60%). Results Compressed file sizes decreased from 12 to 83 MB to 0.03 to 2.3 MB (1:1051-1:26 reduction ratios). Mean SD of differences was 0.81 for intraobserver variability (uncompressed and digital video files). Compared with uncompressed files, only the DivX mean score at 35% ( P = .04) and 60% ( P = .001) compression was significantly reduced. At subcategory analysis, these differences were still significant for gray-scale and fundamental imaging but not for color or second harmonic tissue imaging. Original image quality, session sequence, compression grade, and bitrate were all independent determinants of mean score. Conclusions Our study supports use of MPEG-4 algorithms to greatly reduce echocardiographic file sizes, thus facilitating archiving and transmission. Quality evaluation studies should account for the many independent variables that affect image quality grading.

In chronic heart failure (HF), the alveolar-capillary membrane undergoes a remodeling process that negatively affects gas exchange. In case of alveolar-capillary gas diffusion impairment, arterial desaturation (SaO2) is rarely observed in HF patients. At play are 3 factors: overall pulmonary diffusing capacity (assessed as lung diffusion for CO, DLCO), global O2 consumption (VO2) and alveolar (A) to arterial (a) pO2 gradient (AaDO2). In 100 consecutive stable HF patients, DLCO, resting respiratory gases and arterial blood gases were measured to determine VO2, paO2, pAO2 and AaDO2. DLCO was poorly but significantly related to AaDO2. The correlation improved after correcting AaDO2 for VO2 (p

Transmitral color Doppler early diastolic flow propagation velocity (Vp) has been correlated with the left ventricular (LV) relaxation time constant tau in dilated cardiomyopathy and ischemic heart disease. The aim of this study was to investigate the independent influence of LV systolic function and geometry, and of LV relaxation, on Vp in an unselected outpatient population. We studied 30 normal subjects and 130 patients (hypertensive LV hypertrophy, aortic valve stenosis or prosthesis, hypertrophic cardiomyopathy, coronary artery disease, dilated cardiomyopathy, aortic or mitral valve regurgitation). In all, we noninvasively measured LV geometry, mass, systolic function, wall motion dyssynergy, and diastolic function (abnormal relaxation or restrictive LV Doppler filling patterns). The Vp was similar in normal subjects and in patients (51 +/- 14 vs 53 +/- 25 cm/s). In normal subjects, the determinants of Vp at multiple regression analysis were isovolumic relaxation time, 2-dimensional cardiac index, and mitral E-wave velocity-time integral. In all, the main determinants were LV ejection fraction, percent of segmental wall dyssynergy, and isovolumic relaxation time and age. The Vp was highest in hypertrophic (75 +/- 25 cm/s, p

Aims: The purposes of this study were to compare the accuracy of multiplane vs. biplane transoesophageal echocardiography (TEE) in the diagnosis of aortic dissection and aortic intramural haematoma, and to test whether these techniques provide all the diagnostic information required to make management decisions. Methods and Results: Fifty-eight consecutive patients with clinically suspected aortic dissection were studied with multiplane TEE; all cases who required surgery underwent intraoperative monitoring with multiplane TEE. The following multiplane TEE data were analysed: the angle between current and 0° plane at which each view was obtained; the success rate in the evaluation of true and false lumen, entry tear, coronary artery involvement, aortic regurgitation, pericardial effusion. Advantages of multiplane over biplane TEE have been evaluated by the demonstration of usefulness of views obtained in planes other than 0°–20° or 70°–110°, assuming that with manipulation of a biplane probe a 20° arc could be added to the conventional horizontal and vertical planes. On the basis of TEE findings, aortic dissection was confirmed in 36 cases (18 type A, 12 type B, six intramural haematoma). The specificity and sensitivity of TEE in terms of the presence or absence of aortic dissection or intramural haematoma were 100%. An additional clinical value of multiplane over biplane TEE in the evaluation of ascending aorta, aortic arch, entry tears and coronary artery involvement was demonstrated. All cases with type A aortic dissection or intramural haematoma involving the ascending aorta had an operation that was performed immediately after the diagnosis (hospital mortality, 13%). Patients with type B aortic dissection were treated medically; 25% of these cases were operated later (hospital mortality, 0%). Conclusions: Multiplane and biplane TEE have excellent and similar accuracies in the evaluation of aortic dissection and intramural haematoma. Multiplane TEE improves the visualization of coronary arteries, aortic arch and entry tears; it appears to be an ideal method as the sole diagnostic approach before surgery in type A aortic dissection.

Background An increase in sympathetic drive to the heart and the peripheral circulation characterizes mild and severe essential hypertension. However, it remains unsettled whether sympathetic cardiovascular influences are potentiated in true resistant hypertension (RHT). Methods In 32 RHT patients treated with 4.6 ± 0.3 drugs (mean ± SEM) and aged 58.6 ± 2.1 years, 35 non-resistant treated hypertensives (HT) and 19 normotensive controls (NT), all age-matched with RHT, we measured clinic, 24-hour ambulatory and beat-to-beat blood pressures (BP), heart rate (HR, EKG), muscle sympathetic nerve traffic (MSNA, microneurography) and spontaneous baroreflex MSNA-sensitivity. Results BP values were markedly greater in RHT patients than in NT and HT (172.2 ± 1.7/100.7 ± 1.2 vs 132.1 ± 1.3/82.1 ± 0.9 and 135.5 ± 1.2/83.6 ± 0.9 mm Hg, P < 0.01). This was paralleled by a significant and marked increase in MSNA (87.8 ± 2.0 vs 46.8 ± 2.6 and 59.3 ± 1.7 and bursts/100 heartbeats, P < 0.01). In multiple regression analysis the MSNA increase observed in RHT was significantly related to hemodynamic, hormonal and metabolic variables. It was also significantly related to plasma aldosterone values as well as spontaneous baroreflex MSNA-sensitivity, which were the variables that at the multivariate analysis were more closely related to the adrenergic activation of RHT after adjustment for confounders, including antihypertensive treatment (r2partial = 0.04405 and r2partial = 0.00878, P < 0.05 for both). Conclusions These data represent the first evidence that RHT is a state of marked adrenergic overdrive, greater for magnitude than that detectable in HT. They also suggest that impaired baroreflex mechanisms, along with hemodynamic and neurohumoral factors, may be responsible for the phenomenon.

Several β-blockers, with different pharmacological characteristics, are available for heart failure (HF) treatment. We compared Carvedilol (β1-β2-α-blocker), Bisoprolol (β1-blocker), and Nebivolol (β1-blocker, NO-releasing activity).Sixty-one moderate HF patients completed a cross-over randomized trial, receiving, for 2 months each, Carvedilol, Nebivolol, Bisoprolol (25.6 ± 12.6, 5.0 ± 2.4 and 5.0 ± 2.4 mg daily, respectively). At the end of each period, patients underwent: clinical evaluation, laboratory testing, echocardiography, spirometry (including total DLCO and membrane diffusion), O2/CO2 chemoreceptor sensitivity, constant workload, in normoxia and hypoxia (FiO2=16%), and maximal cardiopulmonary exercise test.No significant differences were observed for clinical evaluation (NYHA classification, Minnesota questionnaire), laboratory findings (including kidney function and BNP), echocardiography, and lung mechanics. DLCO was lower on Carvedilol (18.3 ± 4.8*mL/min/mmHg) compared to Nebivolol (19.9 ± 5.1) and Bisoprolol (20.0 ± 5.0) due to membrane diffusion 20% reduction (*=p0.0001). Constant workload exercise showed in hypoxia a faster VO2 kinetic and a lower ventilation with Carvedilol. Peripheral and central sensitivity to CO2 was lower in Carvedilol while response to hypoxia was higher in Bisoprolol. Ventilation efficiency (VE/VCO2 slope) was 26.9 ± 4.1* (Carvedilol), 28.8 ± 4.0 (Nebivolol), and 29.0 ± 4.4 (Bisoprolol). Peak VO2 was 15.8 ± 3.6*mL/kg/min (Carvedilol), 16.9 ± 4.1 (Nebivolol), and 16.9 ± 3.6 (Bisoprolol).β-Blockers differently affect several cardiopulmonary functions. Lung diffusion and exercise performance, the former likely due to lower interference with β2-mediated alveolar fluid clearance, were higher in Nebivolol and Bisoprolol. On the other hand, Carvedilol allowed a better ventilation efficiency during exercise, likely via a different chemoreceptor modulation. Results from this study represent the basis for identifying the best match between a specific β-blocker and a specific HF patient.

To assess the effect of chronotropic incompetence on functional capacity in chronic heart failure (CHF) patients, as evaluated as NYHA and peak oxygen consumption (pVO(2) ), focusing on the presence and dose of β-blocker treatment.Nine hundred and sixty-seven consecutive CHF patients were evaluated, 328 of whom were discarded because they failed to meet the study criteria. Of the 639 analyzed, 90 were not treated with β-blockers whereas the other 549 were. The latter were further subdivided in high (n = 184) and low (n = 365) β-blockers daily dose group in accordance with an arbitrary cut-off of 25 mg for carvedilol and of 5 mg for bisoprolol. Failure to achieve 80% of the percentage of maximum age predicted peak heart rate (%Max PHR) or of HR reserve (%HRR) constituted chronotropic incompetence.No differences were found in NYHA or pVO2 between patients with and without β-blockers and, similarly, between high and low β-blocker dose groups. Twenty and sixty-nine percent of not β-blocked patients showed chronotropic incompetence according to %Max PHR and %HRR, respectively, whereas this prevalence rose to 61% and 84% in those on β-blocker therapy. Patients taking β-blockers without chronotropic incompetence, as inferable from both %Max PHR and %HRR, showed higher NYHA and pVO2 regardless of drug dose, whereas, in not β-blocked patients, only %HRR revealed a difference in functional capacity. At multivariable analysis, HR increase during exercise (ΔHR) was the variable most strongly associated to pVO2 (β: 0.572; SE: 0.008; P0.0001) and NYHA class (β: -0.499; SE: 0.001; P0.0001).ΔHR is a powerful predictor of CHF severity regardless of the presence of β-blocker therapy and of β-blocker daily dose.

This review covers the role of three-dimensional (3D) echocardiography in the diagnosis of heart valve disease. Several factors have contributed to the evolution of this technique, which is currently a simple and routine method: rapid evolution in probe and computer technologies, demonstration that 3D data sets allowed more complete and accurate evaluation of cardiac structures, emerging clinical experience indicating the strong potential particularly in valve diseases, volume and function of the two ventricle measurements and several other fields. This report will review current and future applications of 3D echocardiography in mitral, aortic and tricuspid valve diseases underlying both qualitative (morphologic) and quantitative advantages of this technique. (Heart International 2007; 3: 35-41)

We evaluated exercise performance in 14 patients with uncomplicated essential hypertension 1 h after the administration of a single dose of placebo, nifedipine (20 mg), captopril (50 mg), and propranolol (80 mg). Drugs were administered at the same time of day following a randomized, double-blind protocol. Mean resting blood pressure (±SE) was 135±3 mm Hg with placebo administration, 118±4 with captopril, 110±4 with nifedipine, and 115±5 with propranolol and increased with exercise to 163±4, 146±3, 136±4, 136±4, respectively. Oxygen consumption at peak exercise and at ventilatory anaerobic threshold (VAT) was 25.2±1.1 and 18.1 ± 1.0 ml/min/kg with placebo. Only propranolol (—2.3 ml/min/kg) decreased peak exercise oxygen consumption. Oxygen consumption at VAT was reduced by nifedipine and propranolol but unaffected by captopril. The effects on exercise capacity of blood pressure reduction in hypertensive patients are dependent on the drug utilized and are not related to the amount of blood pressure reduction. The lowered oxygen consumption at VAT observed with nifedipine and propranolol, and not with captopril, might be due to an excessive downward shift of the muscle perfusion pressure—oxygen consumption relationship which might take place during exercise.

In untreated patients with uncomplicated essential hypertension, exercise induces an abnormal increase in blood pressure; the influences of this increase on exercise were evaluated by a cardiopulmonary exercise test (CPX) performed in control conditions (step 1) and during acute blood pressure reduction (step 2). Patients were classified as (1) normotensive (resting diastolic blood pressure [BPd] less than 90 mm Hg; n = 14), (2) mildly hypertensive (BPd of 90 to 104 mm Hg; n = 9), and (3) moderately to severely hypertensive (BPd greater than or equal to 105 mm Hg; n = 16). For the three groups, peak mean blood pressure during exercise was 125 +/- 5 mm Hg (mean +/- SEM), 144 +/- 3 mm Hg (p less than 0.01 vs normotensive), and 161 +/- 4 mm Hg (p less than 0.01 vs normotensive and p less than 0.01 vs mild hypertension), respectively. Oxygen consumption (VO2) at peak exercise and at ventilatory anaerobic threshold was 26.1 +/- 1.1 and 17.2 +/- 0.5 ml/min/kg, 25.4 +/- 1.1 and 16.9 +/- 0.8 ml/min/kg, and 26.4 +/- 1.3 and 17.5 +/- 1.2 ml/min/kg in normotensive subjects, those with mild hypertension, and those with moderate to severe hypertension, respectively. Fourteen normotensive subjects, six with mild hypertension, and nine with moderate to severe hypertension participated to step 2 (nifedipine vs placebo, double-blind crossover). Nifedipine reduced blood pressure at rest and at peak exercise in those with hypertension. Peak exercise VO2 was unaffected by nifedipine in both normotensive subjects and those with hypertension. With nifedipine, ventilatory anaerobic threshold occurred earlier and at a lower VO2 in mild and in moderate to severe hypertension (delta VO2 = -1.9 and -2.4 ml/min/kg, respectively). These findings might be due to nifedipine-induced redistribution of blood flow during exercise and might be the reason for the complaint of weakness after blood pressure reduction in hypertensive subjects.

The spread of echocardiography has increased the number of requests for echocardiography and the length of patient waiting lists in National Health Systems. This overuse of echocardiography may also result in a decrease in examination quality because of an excess in workload. The recommended use of guidelines for the requesting of echocardiograms could reduce the demand for this investigation and thus reduce both workload and health care costs.In a prospective study of 520 outpatients in a large tertiary referral center, we analyzed adherence by family physicians and cardiovascular specialists to published guidelines for requesting echocardiograms; the use of a written indication justifying the request for the first and subsequent examinations; the diagnostic outcome; and the clinical utility of each echocardiogram performed.Most echocardiograms (72%) were requested by specialists, follow-ups were frequent (72%), and 14% of these proved normal. Among first examinations, 49% of those requested by family physicians and 36% of those requested by specialists were normal (P = not significant [NS]); in both groups 27% of the requests lacked a written indication. Family physicians requested echocardiograms chiefly for arterial hypertension, palpitations, chest pain, and valve disease, whereas specialists most often requested echocardiograms for checking valve prostheses, ischemic heart disease, and valve disease. The rate of adherence to guidelines (54% vs 52%, P = NS) and clinical utility (60% vs 61%, P = NS) was low and similar for family physicians and specialists. Provision of a written indication for the examination by the requesting physician correlated strongly to the clinical utility of the test (P.001), and adherence of indication to guidelines was the major determinant of clinical utility at logistic regression analysis (P.001).The rate of adherence to guidelines was lower than desirable and similar for family physicians and cardiovascular specialists. Adherence to guidelines and provision of a written specific indication strongly enhanced the value of the echocardiographic investigation.

Tele-echocardiography is not widely used because of lengthy transmission times when using standard Motion Pictures Expert Groups (MPEG)-2 lossy compression algorythms, unless expensive high bandwidth lines are used. We sought to validate the newer MPEG-4 algorythms to allow further reduction in echocardiographic motion video file size. Four cardiologists expert in echocardiography read blindly 165 randomized uncompressed and compressed 2D and color Doppler normal and pathologic motion images. One Digital Video and 3 MPEG-4 compression algorythms were tested, the latter at 3 decreasing compression quality levels (100%, 65% and 40%). Mean diagnostic and image quality scores were computed for each file and compared across the 3 compression levels using uncompressed files as controls. File dimensions decreased from a range of uncompressed 12-83 MB to MPEG-4 0.03-2.3 MB. All algorythms showed mean scores that were not significantly different from uncompressed source, except the MPEG-4 DivX algorythm at the highest selected compression (40%, p=.002). These data support the use of MPEG-4 compression to reduce echocardiographic motion image size for transmission purposes, allowing cost reduction through use of low bandwidth lines.

Background Thrombolysis (T) is an effective therapy for prosthetic valve thrombosis (PVT). Debate still exists as to which clinical or noninvasive finding best predict the result of T. The aim of the study was to investigate the role of fluoroscopy (F) to predict efficacy of T in pts with mitral PVT. Methods We evaluated 17 consecutive pts with bileaflet mitral PVT. F criteria for PVT were: abnormal disc motion and calculated opening angle >25°. T was carried out with tissue-type plasminogen activator (tPA; 100 mg over 3 hours followed by heparin infusion for 24 hours) and was considered successful when normalization of leaflet motion and opening angle occurred. Results were evaluated according to symptom duration (21 days, late PVT) and to F pattern of PVT (blocked leaflet versus hypomobile leaflet). Results F showed disc motion alteration in 24 of 34 leaflets: 8 leaflets were blocked, whereas 16 were hypomobile. Early (12.7±6.1 days, range 3–21) and late (113±114 days, range 28–365) PVT was present in 8 and 7 pts, respectively. Thrombolysis was successful in 20 of 24 leaflets. Blocked leaflet fully recovered only in early PVT (n=4) pts, whereas they remained blocked in late PVT (n=4). On the contrary, in all of the cases with hypomobile leaflet, disc motion normalized regardless duration of symptoms and extent of disc motion reduction. Interestingly, 4 leaflets with late PVT was diagnosed as blocked by trans-thoracic (TTE). F showed a residual disc movement in all: they fully recovered after T. Two pts with late PVT had both leaflets affected (1 blocked +1 hypomobile); although blocked leaflet did not respond to T, the normalization of hypomobile significantly improved clinical condition. Conclusions F can predict result of T in mitral PVT. PVT with F evidence of hypomobile leaflet always recovers regardless of symptom duration and extent of disc motion reduction, suggesting that the small amount of thrombus needed to interfere with discs motion in bileaflet prostheses remains sensitive to T even after a long time. PVT with F evidence of blocked leaflet has a favorable response to T only in case of early PVT. Late PVT with blocked leaflet does not respond to T, suggesting a larger and stratified thrombus and the coexistence of pannus and, in our series, always required surgery. However, if a hypomobile leaflet coexists, T may be used to restore normal movement of hypomobile leaflet so that to improve patient clinical and hemodynamic condition before operation.

Objective Blockade of bradykinin breakdown and enhancement of prostaglandin release probably participate in the antihypertensive activity of angiotensin converting enzyme (ACE) inhibitors. Cyclooxygenase blockers may attenuate the efficacy of ACE inhibitors by interfering with prostaglandin synthesis, and patients taking aspirin may not benefit from ACE inhibition. This study was designed to evaluate the incidence of the counteractive phenomenon and to define minimal aspirin dosage that causes an antagonistic effect. Methods These were 26 patients with mild to moderate hypertension (group 1) and 26 patients with severe untreated primary hypertension (group 2). Enalapril (20 mg twice a day) was used as a single drug in group 1 and was added to the combination of long-acting nifedipine (30 mg/day) and atenolol (50 mg/day) in group 2. Aspirin was tested at doses of 100 and 300 mg/day, and an attenuation of more than 20% of the mean blood pressure decrease produced by enalapril was the criteria that defined antagonism. Results The 100 mg dose was ineffective. However, 300 mg aspirin had an antagonistic effect in 57% of patients in group 1 and 50% of patients in group 2: mean arterial pressure was lowered by 63% and 91% less, respectively. Results were independent of the drug administration order. In “responders,” aspirin significantly attenuated the renin rise associated with ACE inhibition. Conclusions These findings suggest that a number of ACE-inhibited patients are susceptible to 300 mg/day aspirin, regardless of hypertension severity. Antagonism may be mediated through prostaglandin inhibition according to predominance, in an individual patient, of prostaglandin activation (also as a renin secretory stimulus) or angiotensin blockade by enalapril. Clinical Pharmacology & Therapeutics (1998) 63, 79–86; doi

s S53 487 Early changes of left atrial reservoir function after cardioversion of paroxysmal atrial fibrillation predict relapse of arrhythmia. P. Barbier, R. Chiodelli, M. Alimento, E. Assanelli, G. Marenzi, M.D. Guazzi. Centro Cardiologico Fondazione Monzino, IRCCS, Milan, Italy Atrial fibrillation (AF) causes systolic and diastolic left atrial (LA) dysfunction. Extent of LA systolic stunning after cardioversion of AF have been evaluated, but do not predict recurrence of AF. Aim: to assess LA diastolic (reservoir) function after cardioversion of AF, as predictor of AF relapse 1 month after electrical cardioversion. Methods: we studied 27 patients with paroxysmal AF > 1 month duration. Echocardiograms were perfomed 24 hours before (baseline) and 1 hour, 24 hours, 15 days and 30 days after cardioversion. We measured LA reservoir as the difference between LA maximum and minimum biplane volumes (ml), and LA systolic function (%) as: [(LA end-diastolic, at ECG P wave, volume minimum LA volume)/enddiastolic volume]. Results: after 1 month, sinus rhythm was maintained in 11 (group 1, 41%), and AF relapsed in 16 (group 2, 59%; 2 within 24 hours, 13 within 15 and 1 within 30 days) patients. Associated heart diseases, AF duration, and baseline left ventricular mass index and systolic function, LA biplane maximum (group 1: 90±28 ml, group 2: 90±19, p=ns) volume, and estimated right ventricular systolic pressure were similar in the 2 groups. Baseline LA reservoir was similarly greatly reduced (when compared to value at 30 days post cardioversion of group 1) in both groups (group 1: 16±6 vs 28±7 ml, p

In this study, we tested the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension. The hypothesis took origin from the following two considerations: alveolar hypoxia constricts the pulmonary vessels by enhancing the Ca2+ penetration across sarcolemma of the smooth muscle cells and systemic high blood pressure is associated with an elevation of tone and reactivity of the lung vessels, which seems to depend on an excessive cytosol free Ca2+ concentration due to alterations in sodium handling and in the Na+-Ca2+ exchange system. These considerations suggest the possibility that the disorders in the biochemistry of smooth muscle contraction in hypertension facilitate the rise of cytosol Ca2+ concentration during alveolar hypoxia, thus resulting in a potentiation of the vasoconstrictor properties of this stimulus. In 43 hypertensive and 17 normotensive men, pulmonary arteriolar resistance has been evaluated during air respiration and after 15 minutes of breathing 17%, 15%, and 12% oxygen in nitrogen. Curves relating changes in pulmonary arteriolar resistance to oxygen breathing contents had similar configuration in the two populations but in hypertension were steeper and significantly shifted to the left, reflecting a lower threshold and an enhanced reactivity. This pattern was not related to differences in severity of the hypoxic stimulus, plasma catecholamine concentration, or hypocapnia and respiratory alkalosis induced by hypoxia and probably was not mediated through alpha-receptor activation. Calcium channel blockade with nifedipine was able to almost abolish both the normotensive and the hypertensive pulmonary vasoconstriction reaction. These findings support the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

In hypertension, coronary flow is augmented and oxygen balance is adequate despite an increase in coronary resistance. For the maintenance of flow in the presence of and after regression of ventricular hypertrophy, the ratio of pressure and ventricular mass must remain normal. Coronary reserve would be altered if treatment normalized pressure but not ventricular mass or if pressure were lowered too fast. We investigated 42 patients with primary hypertension. In 28 (Group I) left ventricular mass index (by ultrasound) was within the mean value +2 SD (96 + 38 g/m2) of 145 controls and exceeded these values in the remaining 14 patients (Group 2). The diastolic pressure was lowered rapidly to between 85 and 90 mm Hg with two potent vasodilators, nifedipine (sublingually) and nitroprusside, while a 12-lead electrocardiogram was recorded continuously. During both tests, seven patients in Group 2 (responders) showed inversion of normal T waves, in lead I, aVL, and V3-6. These changes waxed and waned in parallel with the pressure fall and recovery and were not attributable to alterations in adrenergic tone, conduction disturbances, variations, or group differences in the QRS axis, QTc interval, heart rate, left ventricular fractional shortening, wall stress, rate of dimension increase in early diastole, or isovolumic relaxation. A "steal phenomenon'' or passive collapse in compliant coronary lesions during vasodilatation seems unlikely; in fact, patients were free from coronary symptoms, and the electrocardiographic alterations occurred only in seven patients in Group 2, who had a greater left ventricular mass index and required a larger pressure drop to return the diastolic pressure to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Background KII ACE, the enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the lungs; its blockade reduces exposure to angiotensin II and enhances exposure to prostaglandins generated by local kinin hyperconcentration. Our hypothesis is that ACE inhibitors improve pulmonary function in chronic heart failure (CHF) by readjusting lung vessel tone and permeability or alveolar–capillary membrane diffusion. Methods and Results In 16 CHF patients and 16 normal volunteers or mild untreated hypertensives, pulmonary function and exercise tests with respiratory gas analysis were assessed on placebo, enalapril (10 mg BID), enalapril plus aspirin (325 mg/d), or aspirin, in random order and double blind, for 15 days each. In CHF, enalapril increased pulmonary carbon monoxide diffusion (DLCO), oxygen consumption (V̇ o 2 ), and exercise tolerance and reduced the ratio of dead space to tidal volume (V d /V t ) and the ventilatory equivalent for carbon dioxide production V̇ e /V̇ co 2 ). On enalapril, V̇ o 2 ( r =.80, P d /V t ( r =−.69, P =.003) changes from placebo correlated with those in DLCO. These effects were inhibited by aspirin and were absent in control subjects. In 8 additional patients, hydralazine–isosorbide dinitrate, as an alternative treatment for reducing pulmonary capillary wedge pressure (PCWP) and increasing exercise capacity, were more effective than enalapril for the PCWP but did not affect DLCO and V̇ e /V̇ co 2 ; amelioration in V̇ o 2 and V d /V t was unrelated to DLCO and was not modified by aspirin. Conclusions ACE inhibition improved pulmonary diffusion in CHF. Hydralazine–isosorbide dinitrate failed to provide this result. Counteraction by aspirin, a prostaglandin inhibitor, bespeaks prostaglandin participation while on enalapril that might readjust capillary permeability or alveolar–capillary membrane diffusion.