The ratio of tricuspid regurgitation velocity (TRV) to the time-velocity integral of the right ventricular outflow tract (TVIRVOT) has been studied as a reliable measure to distinguish elevated from ...normal pulmonary vascular resistance (PVR). The equation TRV/TVIRVOT × 10 + 0.16 (PVRecho) has been shown to provide a good noninvasive estimate of PVR. However, its role in patients with significantly elevated PVR (> 6 Wood units WU) has not been conclusively evaluated. The aim of this study was to establish the validity of the TRV/TVIRVOT ratio as a correlate of PVR. The role of TRV/TVIRVOT was also compared with that of a new ratio, TRV(2)/TVIRVOT, in patients with markedly elevated PVR (>6 WU).
Data from five validation studies using TRV/TVIRVOT as an estimate of PVR were compared with invasive PVR measurements (PVRcath). Multiple linear regression analyses were generated between PVRcath and both TRV/TVIRVOT and TRV(2)/TVIRVOT. Both PVRecho and a new derived regression equation based on TRV(2)/TVIRVOT: 5.19 × TRV(2)/TVIRVOT - 0.4 (PVRecho2) were compared with PVRcath using Bland-Altman analysis. Logistic models were generated, and cutoff values for both TRV/TVIRVOT and TRV(2)/TVIRVOT were obtained to predict PVR > 6 WU.
One hundred fifty patients remained in the final analysis. Linear regression analysis between PVRcath and TRV/TVIRVOT revealed a good correlation (r = 0.76, P < .0001, Z = 0.92). There was a better correlation between PVRcath and TRV(2)/TVIRVOT (r = 0.79, P < .0001, Z = -0.01) in the entire cohort as well as in patients with PVR > 6 WU. Moreover, PVRecho2 compared better with PVRcath than PVRecho using Bland-Altman analysis in the entire cohort and in patients with PVR > 6 WU. TRV(2)/TVIRVOT and TRV/TVIRVOT both predicted PVR > 6 WU with good sensitivity and specificity.
TRV/TVIRVOT is a reliable method to identify patients with elevated PVR. In patients with TRV/TVIRVOT > 0.275, PVR is likely > 6 WU, and PVRecho2 derived from TRV(2)/TVIRVOT provides an improved noninvasive estimate of PVR compared with PVRecho.
Objectives
We aimed to summarize the evidence for periprocedural and long‐term strategies to both minimize the bleeding risk and ensure sufficient anticoagulation and antiaggregation in hemophilia ...patients undergoing coronary angiography with or without percutaneous coronary interventions (PCI).
Background
Hemophilia patients undergoing coronary angiography and PCI are at risk of bleeding due to deficiency of the essential clotting factors VIII or IX combined with the need of peri‐interventional anticoagulation and antiaggregation and dual antiplatelet therapy (DAPT) after PCI.
Methods
We report on a patient with moderate hemophilia B undergoing single‐vessel PCI with administration of factor IX concentrate during the procedure and during the 1‐month DAPT period. In addition, a systematic review of patients (n = 54, mean age 58 ± 10 years) with hemophilia A (n = 45, 83%) or B (n = 9, 17%) undergoing coronary angiography with or without PCI is presented.
Results
Peri‐interventional factor substitution was performed in the majority (42 of 54, 78%) but not all patients. In 38 of 54 (70%) patients undergoing coronary angiography, PCI with balloon dilation (n = 5), bare metal (n = 31), or drug‐eluting stents (n = 2) was performed. For PCI unfractioned heparin (n = 24), low molecular weight heparin (n = 2), bivalirudin (n = 4), or no periprocedural anticoagulation at all (n = 8) were used. PCI was successful in all cases. After stenting, the majority (28 of 33; 85%) was treated with DAPT (median duration 1 month). Major periprocedural bleeding episodes occurred in 3 of 54 (6%) patients. Bleeding during follow‐up occurred in 11 of 54 (20%) patients.
Conclusions
Coronary angiography and PCI in patients with hemophilia are effective and safe when applying individualized measures to prevent bleeding.
In patients with aortic and/or mitral valve disease the presence of pulmonary hypertension (PH) indicates a decompensated state of the disease with left ventricular and left atrial dysfunction and ...exhausted compensatory mechanism, i.e., a state of heart failure. Pulmonary hypertension in this context is the consequence of the backwards transmission of elevated left atrial pressure. In this form of PH, pulmonary vascular resistance is initially normal (isolated post-capillary PH). Depending on the extent and chronicity of left atrial pressure elevation additional pulmonary vascular remodeling may occur (combined pre- and post-capillary PH). Mechanical interventions for the correction of valve disease often but not always reduce pulmonary pressures. However, the reduction in pulmonary pressures is often modest, and persistent PH in these patients is common and a marker of poor prognosis. In the present review we discuss the pathophysiology and clinical impact of PH in patients with aortic and mitral valve disease, the comprehensive non-invasive and invasive diagnostic approach required to define treatment of PH, and recent insights from mechanistic studies, registries and randomized studies, and we provide an outlook regarding gaps in evidence, future clinical challenges, and research opportunities in this setting.
Heart failure with preserved left ventricular ejection fraction (HFpEF) is a common and very important disease entity because of its association with frequent repeat hospitalization and high ...mortality. Hallmarks of the underlying pathophysiology include a small left ventricular cavity due to concentric remodeling, impaired left ventricular compliance and left atrial dysfunction. This leads to an increase in left atrial and pulmonary pressure on exertion and in advanced stages of the disease already at rest with consecutive exertional dyspnea and exercise intolerance. Additional cardiovascular mechanisms including atrial fibrillation, chronotropic incompetence and coronary artery disease as well as non-cardiac co-morbidities contribute to a variable extent to the clinical picture. The diagnostic work-up is demanding and complex but the concepts have significantly improved during the last years. The study results of the Sodium Glucose cotransporter-2 inhibitors (SGLT-2-inhibitors) have revolutionized the treatment of HFpEF. In the present article, we provide an overview about the current understanding of the pathophysiology of HFpEF, the principles of the diagnostic pathways and a summary of the intervention studies in the field, and we propose an approach for the treatment in clinical practice.
Background
In aortic stenosis (AS), left ventricular hypertrophy (LVH) is the response to pressure overload and represents the substrate for a maladaptive cascade, the so‐called AS‐related cardiac ...damage. We hypothesized that in AS patients electrocardiogram (ECG) LVH not only predicts echocardiography LVH but also other noninvasive and invasive markers of cardiac damage and prognosis after aortic valve replacement (AVR).
Methods
In 279 patients with severe AS undergoing ECG, echocardiography, and cardiac catheterization before AVR, the Sokolow‐Lyon index, the Cornell product, the Romhilt‐Estes score, and the Peguero‐Lo Presti score were assessed.
Results
The mean left ventricular mass index was 109 ± 34 g/m2, and 131 (47%) patients had echocardiography LVH. The areas under the receiver operator characteristics curve (AUC) for the Sokolow‐Lyon index, the Cornell product, the Romhilt‐Estes score, and the Peguero‐Lo Presti score for the prediction of echocardiography LVH were 0.59, 0.70, 0.63, and 0.65. The Peguero‐Lo Presti score had the numerically greatest AUC for the prediction of left ventricular end‐diastolic pressure >15 mmHg, mean pulmonary artery wedge pressure >15 mmHg, pulmonary vascular resistance >3 Wood units, mean right atrial pressure >14 mmHg, and stroke volume index <31 mL/m2. After a median follow‐up of 1365 (interquartile range: 931–1851) days after AVR only the Peguero‐Lo Presti score was significantly associated with all‐cause mortality hazard ratio: 1.24 (95% confidence interval: 1.01–1.54); per 1 mV increase; p = .045.
Conclusions
Among severe AS patients, the Peguero‐Lo Presti score is associated with abnormalities in cardiac structure including LVH, invasive measures of cardiac damage, and long‐term mortality after AVR.
In 279 severe AS patients undergoing ECG, echocardiography, and cardiac catheterization, the Peguero‐Lo Presti score and three other LVH scores were assessed. The Peguero‐Lo Presti score had the greatest AUC for the prediction of key hemodynamics. After a median post‐AVR follow‐up of 1365 days only the Peguero‐Lo Presti score was significantly associated with mortality.
This study sought to identify sex differences in central and peripheral factors that contribute to the pathophysiology of heart failure with preserved ejection fraction (HFpEF) by using complementary ...invasive hemodynamic and echocardiographic approaches.
Women are overrepresented among patients with HFpEF, and there are established sex differences in myocardial structure and function. Exercise intolerance is a fundamental feature of HFpEF; however, sex differences in the physiological determinants of exercise capacity in HFpEF are yet to be established.
Patients with exertional intolerance with confirmed HFpEF were included in this study. Evaluation of the subjects included resting and exercise hemodynamics, echocardiography, and mixed venous blood gas sampling.
A total of 161 subjects included 114 females (71%). Compared to males, females had a higher pulmonary capillary wedge pressure (PCWP) indexed to peak exercise workload (0.8 0.5 to 1.2 mm Hg/W vs. 0.6 0.4 to 1 mm Hg/W, respectively; p = 0.001) and lower systemic (1.1 0.9 to 1.5 ml/mm Hg vs. 1 0.7 to 1.2 ml/mm Hg, respectively; p = 0.019) and pulmonary (2.9 2.2 to 4.2 ml/mm Hg vs. 2.4 1.9 to 3 ml/mm Hg, respectively; p = 0.032) arterial compliance at exercise. Mixed venous blood gas analysis demonstrated a greater rise in lactate indexed to peak workload (0.05 0.04 to 0.09 mmol/l/W vs. 0.04 0.03 to 0.06 mmol/l/W, respectively; p = 0.007) in women compared to men. Women had higher mitral inflow velocity to diastolic mitral annular velocity at early filling (E/e') ratios at rest and peak exercise, along with a higher ejection fraction and smaller ventricular dimensions.
Women with HFpEF demonstrate poorer diastolic reserve with higher echocardiographic and invasive measurements of left ventricular filling pressures at exercise, accompanied by lower systemic and pulmonary arterial compliance and poorer peripheral oxygen kinetics.
Spontaneous coronary artery dissection (SCAD) is an increasingly diagnosed cause of acute myocardial infarction. However, there is still a limited number of larger cohorts with long-term follow-up. ...We report on the largest Swiss single-centre cohort to date, with follow-up of up to 22 years.
We prospectively collected SCAD cases from June 1998 until December 2020. A strategy of systematic follow-up angiography was applied. Information on long-term follow-up was collected up to the end of 2020. Major cardiovascular events (MACE) were defined as all-cause death, non-fatal MI, and non-fatal cardiac arrest.
We identified 105 SCAD patients (mean age 53 ± 11 years, 98 female, 5 peripartum). Presentation was myocardial infarction in all patients. In 102 patients, there was one contiguous dissection. Three patients had two (n = 2) or three (n = 1) non-contiguous dissections. In the majority of patients (n = 97), the primary treatment approach was conservative (dual antiplatelet therapy for 12 months in 90% of patients, statins in 91%). Seven patients were treated with percutaneous coronary intervention (PCI) and one patient underwent bypass surgery. Elective follow-up angiograms were performed in 73 asymptomatic patients after a median follow-up of 6.0 months (interquartile range IQR 5.5-6.5). These showed healing of the dissection (n = 65) or a good result after PCI (n = 5) in 70 patients. Three patients had a persistent dissection but conservative treatment was continued. After a median follow-up of 7.5 years (IQR 3.6-12.5) (longest follow-up: 22.5 years) there were 15 MACE. Five MACE occurred within 30 days of the index event: death following catastrophic peripartum left main SCAD (n = 1), out-of-hospital cardiac arrest with successful resuscitation 16 days after SCAD (n = 1), ST-segment elevation myocardial infarction due to occlusion of the dissected artery 10 hours after the index angiogram with subsequent PCI (n = 1), SCAD of a second vessel 8 days after the index SCAD (n = 1), and non-ST-segment elevation myocardial infarction with persistent, multisite SCAD 10 days after the index event (n = 1). There were 10 late MACE, including myocardial infarction and recurrent SCAD (different vessel/lesion) a median of 7.6 years (IQR 3.9-9.6) after the index event in eight patients and death with unclear cause in two patients.
This SCAD series highlights its highly variable clinical course during the acute phase and in the long term. Although most SCAD patients can be treated conservatively with subsequent healing of the dissection and good clinical outcome, there are also patients with dramatic acute presentation or MACE several years after the initial presentation.
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