Early echocardiographic findings in patients hospitalized for COVID-19 pneumonia: a prospective, single center study.

BACKGROUND: Cardiac dysfunction, mainly assessed by biomarker alterations, has been described in COVID-19 infection. However, there are still areas of uncertainty regarding its effective role in disease evolution. Aim of this study was to evaluate early echocardiographic parameters in COVID pneumonia and their association with severity disease and prognosis. METHODS: An echocardiographic examination was performed within 72 h from admission in 64 consecutive patients hospitalized for COVID-19 pneumonia in our medium-intensity care unit, from March 30th to May 15th 2020. Six patients were excluded for inadequate acoustic window. RESULTS: Fifty-eight consecutive patients were finally enrolled, with a median age of 58 years. Twenty-two (38%) were classifiable as severe COVID-19 disease. Eight out of 58 patients experienced adverse evolution (six died, two were admitted to ICU and received mechanical ventilation), all of them in the severe pneumonia group. Severe pneumonia patients showed higher troponin, IL-6 and D-Dimer values. No significant new onset alterations of left and right ventricular systolic function parameters were observed. Patients with severe pneumonia showed higher mean estimated systolic pulmonary artery pressure (sPAP) (30.7 ± 5.2 mmHg vs 26.2 ± 4.3 mmHg, p = 0.006), even if in the normality range values. No differences in echocardiographic parameters were retrieved in patients with adverse events with respect to those with favorable clinical course. CONCLUSION: A mild sPAP increase in severe pneumonia patients with respect to those with milder disease was the only significant finding at early echocardiographic examination, without other signs of new onset major cardiac dysfunction. Future studies are needed to deepen the knowledge regarding minor cardiac functional perturbation in the evolution of a complex systemic disorder, in which the respiratory involvement appears as the main character, at least in non-ICU patients.

Peripartum cardiomyopathy in a COVID-19-infected woman: differential diagnosis with acute myocarditis-A case report from a Hub Institution during the COVID-19 outbreak.

We report the case of a healthy 35-year-old woman who had experienced a flu-like syndrome during the week before childbirth and heart failure symptoms 10 days before the current hospitalization and presented to our emergency department with clinical signs of congestive heart failure, echocardiographic evidence of a severely dilated and hypokinetic heart, laboratory evidence of SARS-CoV-2 disease, and radiologic findings consistent with both virus-related pneumonia and heart failure. Early cardiac magnetic resonance was crucial for the diagnosis of postpartum cardiomyopathy and for the exclusion of virus-related myocarditis, allowing us to decide on a prudent and supportive clinical approach.

Remission of left ventricular systolic dysfunction and of heart failure symptoms after cardiac resynchronization therapy: temporal pattern and clinical predictors.

BACKGROUND: The aim of the study was to determine whether cardiac resynchronization therapy (CRT) may induce a heart failure (HF) remission phase (recovery to New York Heart Association functional class I-II and regression of left ventricular [LV] dysfunction: LV ejection fraction [EF] > or = 50%) and to define the incidence and predictors of such a process. METHODS: Cardiac resynchronization therapy devices were successfully implanted in 520 consecutive HF patients from 1999 to 2006 (mean age 66 years, 82% male sex, New York Heart Association class > or = II, LVEF 28%, QRS 164 milliseconds, 6-minute hall walk distance 302 m) at our institution. Follow-up data were prospectively collected every 3 to 6 months. Continuous variables were stratified in tertiles. RESULTS: Over a median follow-up of 28 months, 26% of patients achieved LV remission (rate: 16 per 100 person-years). At univariate analysis, female sex (P = .032), non-coronary artery disease (CAD) etiology (P < .001), mitral regurgitation < 2/4 (P = .022), higher EF tertile (P < .001), lower diameter and volume tertiles (both P < .001), previous conventional right ventricle pacing (P = .029), and post-CRT-paced QRS (P = .008) predicted remission. At multivariate analysis, non-CAD etiology, LVEF 30% to 35%, and LV end-diastolic volume < 180 mL were strongly associated with HF remission phase (all P < .001). Concomitance of these 3 factors yielded a significantly higher remission rate compared with either no or only 1 factor (respectively, 60 vs 7 and 11 per 100 person-years, P < .001). CONCLUSIONS: Cardiac resynchronization therapy induces HF remission phase in 26% of patients, even after 3 years. Non-CAD etiology and moderately compromised LV function at baseline may easily predict this process.

Usefulness of three-dimensional echocardiographic reconstruction of the Amplatzer septal occluder in patients undergoing atrial septal closure.

Eighty-eight patients referred for transcatheter closure of atrial septal or patent foramen ovale defects underwent 3-dimensional transesophageal echocardiography to correlate preclosure anatomy with the morphology and positioning of the atrial septal occluder. Despite the effectiveness of the trancatheter closure and absence of complications, 2 linear indentations of the aortic root by the 2 discs of the device were clearly demonstrated in 16 cases, suggesting caution in the choice of very large occluders.

Initial experience with a new on-line transthoracic three-dimensional technique: assessment of feasibility and of diagnostic potential.

BACKGROUND: Despite its wide diagnostic potential, three-dimensional (3D) echocardiography is a quite rarely employed technique. The ideal method to obtain transthoracic 3D imaging is on-line 3D echocardiography, but first-generation real-time instruments had technical limitations. A new on-line 3D technology which allows true real-time volume rendering of the cardiac anatomy has been recently introduced and its feasibility and diagnostic advantages have been evaluated in the clinical setting. METHODS: The system utilizes a "matrix" transducer with a dedicated software. It allows instantaneous acquisition and rendering on-line 3D images and interactive manipulation of 3D data. Eighty-three adult patients with various cardiac pathologies underwent on-line 3D echocardiography. Long- and short-axis views of the aorta, mitral valve and left ventricle and surgical views of these structures were attempted. The duration of acquisition and reconstruction, and the quality and incremental clinical value of 3D images in comparison with two-dimensional imaging were annotated. RESULTS: The mean time of 3D examination was 10 +/- 5 min; the mean number of acquisitions was 10.8 per patient. The quality of the 3D images was optimal in 39%, good in 37%, sufficient in 19%, and insufficient in 5% of the patients. In all cases at least one optimal or good live 3D image was obtained from the parasternal and apical views. The reconstruction of surgical or en face views was easily and rapidly (1-2 min) achieved by two experts in 3D echocardiography. The additional clinical values of 3D vs two-dimensional imaging was demonstrated in 7 patients with mitral valve disease, 3 with aortic valve pathology, and 3 with congenital heart disease. Several on-line 3D images that have not correspondence with two-dimensional echocardiography were reconstructed, creating projections dedicated to the diagnostic goal. CONCLUSIONS: On-line 3D echocardiography can be easily performed in adult patients and allows for unique planes and projections. The instant rendering of 3D images facilitates the recognition of cardiac structures and increases the diagnostic potential of transthoracic echocardiography.

Normalization for peak oxygen uptake increases the prognostic power of the ventilatory response to exercise in patients with chronic heart failure.

BACKGROUND: Peak exercise oxygen uptake (peak VO2) and ventilation to CO2 production (VE/VCO2) slope are established prognostic indicators in patients with chronic heart failure (CHF). A high VE/VCO2 slope, however, does not take into account the level of physical performance as expressed by peak VO2. We hypothesized that the prognostic value of a high VE/VCO2 slope may be improved by normalization for peak VO2 (VE/VCO2/VO2). METHODS: One hundred patients with CHF underwent pulmonary function tests at rest (spirometry and lung diffusion capacity) and maximal cardiopulmonary exercise testing. The prognostic value of VE/VCO2 slope, peak VO2 and VE/VCO2/VO2 was probed prospectively. RESULTS: Twenty-one patients died from cardiac reasons during a mean follow-up of 26 +/- 19 months. Nonsurvivors, compared to survivors, showed a lower peak VO2 (13.6 +/- 4.0 vs 17.5 +/- 4.1 mL x min(-1) x kg(-1), P <.01) and a steeper VE/VCO2 slope (43 +/- 11 vs 31.6 +/- 5.0, P <.01). Nonetheless, in patients whose VE/VCO2 slope exceeded 34 (upper normal limit), there was no correlation with peak VO2 (r = -35, P = not significant). Interestingly 35% of them showed a normal exercise performance (peak VO2 > or =18 mL x min(-1) x kg(-1)). At multivariate analysis, the VE/VCO2 slope showed a prognostic power stronger than that of peak VO2; however, the VE/VCO2/VO2 index retained a prognostic power greater than that of both VE/VCO2 slope and peak VO2. A VE/VCO2/VO2 > or =2.4 signaled cases at higher risk. CONCLUSIONS: Discrepancies between VE/VCO2 slope and peak VO2 may generate uncertainty. Normalization of the former by the latter improves outcome prediction and may be considered a simple and effective way for maximizing the clinical applicability of these 2 indicators.

Carvedilol reduces the inappropriate increase of ventilation during exercise in heart failure patients.

STUDY OBJECTIVE: To evaluate the effects of beta-blockers on ventilation in heart failure patients. Indeed, beta-blockers ameliorate the clinical condition and cardiac function of heart failure patients, but not exercise capacity. Because ventilation is inappropriately elevated in heart failure patients due to overactive reflexes from ergoreceptors and chemoreceptors, we hypothesized that beta-blockers can elicit their positive clinical effects through a reduction of ventilation. DESIGN: This was a double-blind, randomized, placebo-controlled study. SETTING: University hospital heart failure unit. PATIENTS AND INTERVENTIONS: While receiving placebo (2 months) and a full dosage of carvedilol (4 months), 15 chronic heart failure patients were evaluated by quality-of-life questionnaire, pulmonary function tests, cardiopulmonary exercise tests with constant workload, and a ramp protocol. RESULTS: Therapy with carvedilol did not affect resting pulmonary function and exercise capacity. However, carvedilol improved the results of the quality-of-life questionnaire, reduced the mean (+/- SD) slope of the minute ventilation (E)/carbon dioxide output (CO(2)) ratio (from 36.4 +/- 8.9 to 31.7 +/- 3.8; p < 0.01) and reduced ventilation at the following times: at peak exercise (from 60 +/- 14 to 48 +/- 15 L/min; p < 0.05); during the intermediate phases of a ramp-protocol exercise; and during the steady-state phase of a constant-workload exercise (from 42 +/- 14 to 34 +/- 13 L/min; p < 0.05, at third min). The end-expiratory pressure for carbon dioxide increased as ventilation decreased. The reduction in the E/CO(2) ratio was correlated with improvement in quality of life (r = 0.603; p < 0.02). CONCLUSIONS: Improvement in the clinical conditions of heart failure patients treated with carvedilol is associated with reductions in the inappropriately elevated ventilation levels observed during exercise.

[Alveolar-capillary dysfunction in heart failure]. / La disfunzione alveolo-capillare nell'insufficienza cardiaca.

Heart failure increases the resistance to gas transfer across the alveolar-capillary interface. In different experimental conditions of vascular capillary injury, peculiar anatomical and functional abnormalities of the alveolar unit have been reported and consist of a disruption of its anatomical configuration and of a loss of fluid-flux regulation and gas exchange efficiency (i.e. "stress failure" of the alveolar-capillary membrane). In heart failure, the pathophysiological relevance of these changes has been only recently appreciated. Alveolar-capillary membrane conductance and capillary blood volume are subcomponents of lung diffusion capacity. A reduction of the former with an increase of the latter and consequent impairment of gas exchange are typical of heart failure syndrome. Alveolar-capillary membrane conductance abnormalities have been shown to be a sensitive index of the underlying lung tissue damage, bring an independent prognostic information and play a significant role in the pathogenesis of exercise limitation and ventilatory abnormalities. This review examines the current knowledge on this topic.

Diabetes worsens pulmonary diffusion in heart failure, and insulin counteracts this effect.

Chronic heart failure (CHF) (hydrostatic stress) and diabetes (basal laminae thickening) share the potentiality of damaging the alveolar-capillary membrane. We investigated 15 control subjects and 3 groups of 15 patients each having type 2 diabetes (Group 1), CHF (Group 2), and diabetes and CHF (Group 3), to probe whether addition of diabetes worsens lung diffusion in CHF and whether insulin counteracts this effect. Compared with control subjects, carbon monoxide diffusing capacity (DL(CO)) and diffusing capacity of the alveolar-capillary membrane at rest were increasingly depressed from Group 1 through Group 3. DL(CO) was lower than predicted in 11 patients each in Groups 1 and 2 and in all patients in Group 3. Regular insulin (10 IU) was ineffective in CHF alone, whereas it improved DL(CO) and diffusing capacity of the alveolar-capillary membrane in diabetes; changes, however, were significantly greater in the patients with both diabetes and CHF (+17.6%, +27.3%) than in those with diabetes alone (+9.2%, +13.1%). Insulin did not affect lung spirometry, volumes, and hemodynamics. Thus, gas transfer is depressed in a number of patients with diabetes or CHF; comorbidity increases the frequency and extent of this disorder. Insulin facilitates diffusion in diabetes, through an influence on alveolar-capillary conductance, and its efficacy is greater in comorbidity; diabetes is more disturbing in patients with CHF and produces a synergistic rather than a simple additive effect.