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Right-parasternal-view (RPV) often provides the best hemodynamic assessment of the aortic-valve-stenosis by echocardiography. However, no detailed study on patients with aortic prosthesis is available. Thus, RPV usefulness is left as an anecdotical notion in this context. We aimed to define feasibility and clinical-impact of RPV before and soon-after percutaneous implantation (TAVI) or surgical (SAVR) aortic-valve-replacement (AVR) for AS. Patients with severe-AS electively referred for AVR between September-2019 and February-2020 were prospectively evaluated. Echocardiographic examinations inclusive of apical and RPV to measure aortic-peak-velocity , gradients and area (AVA) were performed the day before AVR and at hospital discharge and compared by matched-pair-analysis. Forty-seven patients (mean age 79 ± 8 years, 63% female, ejection-fraction 61 ± 6%) referred for SAVR (24 [51%]) or TAVI (23 [49%]) were enrolled. RPV was feasible in 45 patients (96%) before-AVR but in only 32 after-AVR (68%), particularly after SAVR (50%) than TAVI (87% p = 0.005). RPV remained the best acoustic window after TAVI in 75% of cases. Hemodynamic assessment of TAVI, but not SAVR, invariably benefit from RPV versus apical evaluation (aortic-peak-velocity: 2.57 ± 0.39 vs 2.23 ± 0.47 m/sec, p = 0.002; mean gradient: 15 ± 5 vs 12 ± 5 mm Hg, p = 0.01). Five (11%) patients presented severe patient-prosthesis-mismatch, 4 of which were detectable only by RPV. This pilot-experience demonstrates that RPV feasibility is slightly reduced after AVR. RPV can improve the hemodynamic assessment of the prosthetic valve versus apical view, including the detection of patient-prosthesis-mismatch. Furthermore, when RPV is the best acoustic windows in patients with severe AS, it generally remains so after-TAVI., (Copyright © 2020 Elsevier Inc. All rights reserved.)

To examine left ventricular (LV) function in patients after acute myocardial infarction (AMI) and assess its relation to C-reactive protein (CRP) as a measure of the early inflammatory response. We measured the CRP levels early after AMI and correlated them with the early structural and functional cardiac alterations. From November 2002 to December 2007, we prospectively enrolled community subjects who had experienced an AMI, as defined by standardized criteria, measured the CRP level, and obtained an echocardiogram. The study consisted of 514 patients (mean age 67 +/- 15 years, 59% men). CRP was measured early after symptom onset (median 6.1 hours; twenty-fifth to seventy-fifth percentile 2.2 to 11.1). The median CRP level was 4.8 mg/L (twenty-fifth to seventy-fifth percentile 1.8 to 24). The echocardiograms were obtained at a median of 1 day after AMI. The wall motion score index, LV ejection fraction, and LV diameter were similar across the CRP tertiles (all p >0.05). Greater CRP levels were associated with the presence of moderate or severe diastolic dysfunction (p = 0.002) and moderate or severe mitral regurgitation (p <0.001). The association with moderate or severe mitral regurgitation was independent of the clinical characteristics and ST-segment elevation status. In conclusion, at the initial phase of AMI, CRP elevation was associated with the presence and severity of mitral regurgitation and diastolic dysfunction. This suggests that inflammation is related to the ventricular remodeling processes, independently of LV systolic function., (Copyright 2010 Elsevier Inc. All rights reserved.)

Background: There is a paucity of data on the prognostic role of C-reactive protein (CRP) measured after myocardial infarction. We prospectively examined the association of CRP with heart failure and death among patients with myocardial infarction in the community., Methods and Results: All Olmsted County residents who had a myocardial infarction meeting standardized criteria were prospectively enrolled to measure CRP on admission and followed for heart failure and death. A total of 329 consecutive patients (mean age 69 +/- 16 years, 52% men) were enrolled. At 1 year, 28% of patients experienced heart failure and 20% died. There was a strong positive graded association between CRP and the risk of developing heart failure, as well as dying over the period of follow-up (P < .001). Compared with patients in the first tertile, patients in the third tertile of the CRP distribution had a markedly increased risk of heart failure and death independently of age, sex, troponin T, Q wave, comorbidity, previous myocardial infarction, and recurrent ischemic events (adjusted hazard ratio 2.47 [95% confidence interval, 1.27-4.82] for heart failure and 3.96 [95% confidence interval, 1.78-8.83] for death)., Conclusions: These prospective data indicate that among contemporary community subjects with myocardial infarction, heart failure and death remain frequent complications. CRP is associated with a large increase in the risk of heart failure and death, independently of age, sex, myocardial infarction severity, comorbidity, previous myocardial infarction, and recurrent ischemic events. These data suggest that inflammatory processes may play a role in the development of heart failure and death after myocardial infarction independently of other conventional prognostic indicators.

Purpose: Little is known on the prevalence and prognostic importance of diabetes mellitus (DM) among individuals with heart failure (HF) in community-based cohorts., Methods: Within Olmsted County, Minnesota, a random sample of all subjects with a first diagnosis of HF between 1979 and 1999 was validated using Framingham criteria. DM was validated using glycemic criteria., Results: Among 665 subjects with HF (mean age 77+/-12 years, 46% male), 20% had prior DM. Subjects with DM were younger, had greater body mass index (BMI), and lower left ventricular ejection fraction than subjects without diabetes. The prevalence of DM increased markedly over time (3.8% per year; 95% confidence interval [CI], 0.8 to 6.9; P=.024), independently of BMI, particularly in older subjects (odds ratio of having DM in 1999 compared with 1979 was 3.93 [95% CI, 1.57 to 9.83] in subjects > or = 75 years vs. 1.11 [95% CI, .40 to 3.05] in subjects <75 years). Five-year survival was 37% among subjects with DM versus 46% among subjects without (P=.017). The risk of death associated with DM differed markedly according to clinical coronary artery disease (CAD) (P=.025). Subjects with DM and no CAD had a higher risk of death (relative risk [RR]=1.79 [95% CI, 1.33 to 2.41]) than those with CAD (RR=1.11 [95% CI, .81 to 1.51]), independently of age, sex, BMI, renal function, calendar year of HF, comorbidity and EF., Conclusions: Among community-dwelling patients with HF, the prevalence of DM increased markedly over time. DM is associated with a large increase in mortality, particularly among subjects without clinical CAD, underscoring the importance of aggressive management of DM in HF.

Mitral regurgitation after myocardial infarction is the result of multifactorial processes involving local and global left ventricular remodeling. The prevalence of mitral regurgitation varies from 11% to 59%. Published studies differ greatly in design, inclusion criteria, duration of follow-up, and technique of mitral regurgitation assessment. However, they consistently indicate that mitral regurgitation after myocardial infarction carries an adverse prognosis with increased risk of death and heart failure independently of previously known indicators of risk after myocardial infarction. Mitral regurgitation is often clinically silent; therefore, it should be systematically evaluated by echocardiography. Standard color Doppler imaging is a highly sensitive method to detect even mild degrees of ischemic mitral regurgitation. One unique advantage of echocardiography is that it accurately quantifies the severity of mitral regurgitation by measuring the effective regurgitant orifice area and the regurgitant volume using Doppler methodology. Therefore, the evaluation should include precise quantification of the degree of mitral regurgitation to best appraise the ensuing risk. Current medical options rely chiefly on angiotensin converting enzyme-inhibitors and beta-blocker therapy, and surgical approaches offer future promise. Both categories of therapeutic approaches should be evaluated by randomized controlled trials.