Considerations on the naming of myocardial infarctions.

The electrocardiogram is not only an indispensable tool for the diagnosis of myocardial infarction, but also helps in the prediction of its location and extent. However, there is a confusion regarding to the electrocardiographic nomenclature on the naming of infarcting left ventricular segments. This review briefly examines the sources of this confusion and gives some recommendations to avoid them.

The Interplay between Features of Plaque Vulnerability and Hemodynamic Relevance of Coronary Artery Stenoses.

Fractional flow reserve (FFR) may not be immune from hemodynamic perturbations caused by both vessel and lesion related factors. The aim of this study was to investigate the impact of plaque- and vessel wall-related features of vulnerability on the hemodynamic effect of intermediate coronary stenoses. Methods and Results: In this cross-sectional study, patients referred to catheterization laboratory for clinically indicated coronary angiography were prospectively screened for angiographically intermediate stenosis (50-80%). Seventy lesions from 60 patients were evaluated. Mean angiographic stenosis was 62.1 ± 16.3%. After having performed FFR assessment, intravascular ultrasound (IVUS) was performed over the FFR wire. Virtual histology IVUS was used to identify the plaque components and thin cap fibroatheroma (TCFA). TCFA was significantly more frequent (65 vs. 38%, p = 0.026), and necrotic core volume (26.15 ± 14.22 vs. 16.21 ± 8.93 mm3, p = 0.04) was significantly larger in the positively remodeled than non-remodeled vessels. Remodeling index correlated with necrotic core volume (r = 0.396, p = 0.001) and with FFR (r = -0. 419, p = 0.001). With respect to plaque components, only necrotic core area (r = -0.262, p = 0.038) and necrotic core volume (r = -0.272, p = 0.024) were independently associated with FFR. In the multivariable model, presence of TCFA was independently associated with significantly lower mean FFR value as compared to absence of TCFA (adjusted, 0.71 vs. 0.78, p = 0.034). Conclusion: The current study demonstrated that for a given stenosis geometry, features of plaque vulnerability such as necrotic core volume, TCFA, and positive remodeling may influence the hemodynamic relevance of intermediate coronary stenoses.

The Association between Serum Heme Oxygenase-1 Levels and Coronary SYNTAX Score.

AIM: The relationship between heme oxygenase-1 (HO-1) levels and atherosclerosis was investigated in multiple studies. The aim of this study was to establish the relationship between HO-1 levels and coronary SYNergy between percutaneous coronary intervention with TAXus and Cardiac Surgery (SYNTAX) score in patients with stable coronary artery disease (CAD). METHODS: Patients who had been planned to undergo invasive coronary angiography due to a suspected CAD, between the dates of September and December 2019, were included in the study. Serum HO-1 levels were measured from peripheral venous blood. The SYNTAX score was calculated using standard coronary angiography images. Regression analysis was performed to establish the relationship between HO-1 levels and the SYNTAX score. RESULTS: In total, 137 patients were included. The median age was 63 years (IQR: 15), and most of the patients were male (75.2%). The median HO-1 level was 1.44 (IQR: 0.88) ng/mL, and the median SYNTAX score was 6 (IQR: 13). Regression analysis showed that HO-1 is the single most important variable associated with the SYNTAX score (HO-1 levels from 1.01 to 1.87 ng/mL, OR: 6.77, 95% confidence interval 5.18-8.36, p < 0.0001). CONCLUSION: In this study, serum HO-1 levels were significantly associated with the coronary SYNTAX score.

STEMI: A transitional fossil in MI classification?

An important task in emergency cardiology is distinguishing patients with acute coronary occlusion (ACO), who will benefit from emergent reperfusion therapy, from those without ongoing myocyte loss who can be managed with medical therapy and for whom potentially harmful invasive interventions can be deferred. The electrocardiogram is critical in this process. Although the ST-segment elevation myocardial infarction (STEMI)/non-STEMI paradigm is well-established, with "STEMI" representing ACO, its evidence base is poor, and this can have dire consequences. The universally recommended STEMI criteria do not accurately diagnose ACO; in fact, they miss more than one-fourth of the patients with ACO, and also result in a substantial burden of unnecessary catheterization laboratory activations. We here discuss why we believe it is time to change the current STEMI/non-STEMI paradigm.

A new electrocardiographic pattern indicating inferior myocardial infarction.

BACKGROUND: We identified a specific pattern that does not display contiguous ST-segment elevation (STE), indicating acute inferior myocardial infarction (MI) with concomitant critical stenoses on the other coronary arteries. We sought to define the frequency, underlying anatomic substrate, diagnostic power and prognostic implications of this pattern. METHODS: One thousand patients with a diagnosis of non-STEMI were enrolled as the study group. Within the same date range, all patients with inferior STEMI and 1000 patients, who had been excluded for MI (no-MI), were also enrolled. The coronary angiograms were reviewed by two interventional cardiologists, who were blinded to the ECGs. Echocardiographic wall motion bullseye displays and coronary angiography maps were constructed for each group. The dead or alive status was checked from the electronic national database. RESULTS: The final study population consisted 2362 patients. The prespecified ECG pattern was observed in 6.3% (61/966) of the non-STEMI cohort and 0.5% (5/1000) of no-MI patients. These patients had a larger infarct size as evidenced by 24-hour troponin levels, higher frequency of angiographic culprit lesion, and higher frequency of composite acute coronary occlusion endpoint compared to their non-STEMI counterparts. On the other hand, they had a similar in-hospital (5% vs. 4%, respectively; P = 0.675) and one-year mortality compared to the patients with inferior STEMI (11% vs. 8%, respectively; P = 0.311). CONCLUSION: We here define a new ECG pattern indicating inferior MI in patients with concomitant critical lesion(s) in coronary arteries other than the infarct-related artery. Patients with this pattern have multivessel disease and higher mortality.

The established electrocardiographic classification of anterior wall myocardial infarction misguides clinicians in terms of infarct location, extent and prognosis.

BACKGROUND: The currently used scheme for the classification of infarct location and extent in anterior myocardial infarction (MI) is intuitive rather than being evidence-based, and recent evidence suggests that it may be misleading both in anatomic and prognostic sense. MATERIAL AND METHODS: Consecutive patients with the diagnosis of anterior MI were enrolled. All electrocardiograms (ECG) were first classified according to established scheme and then reassessed using newer criteria for angiographic site of occlusion. The site of left anterior descending (LAD) occlusion was determined using multiple angiographic views. Clinic, echocardiographic and angiographic outcomes were compared. RESULTS: A total of 379 anterior MI cases were enrolled, final study population consisted of 267 patients. The established scheme did not predict infarct size or adverse outcomes. Location of the myocardium subtended by the occluded coronary network did not match with the anatomic location as ECG classification implies. Many high-risk patients with proximal LAD were classified as "anteroseptal", whereas the majority of the patients labeled as "extensive anterior MI" had in fact distal occlusions. On the other hand, expert interpretation was fairly accurate in predicting adverse outcomes and the site of angiographic involvement. CONCLUSION: Classifying patients according to the established scheme neither gives prognostic information nor accurately localizes infarction. It should be regarded as obsolete and its use should be abandoned. Instead, the extent of infarction can be inferred from newer criteria provided by the angiographic correlation studies.

A tale of two formulas: Differentiation of subtle anterior MI from benign ST segment elevation.

BACKGROUND: It may sometimes be difficult to differentiate subtle ST-segment elevation (STE) due to anterior myocardial infarction (MI) from benign variant (BV) STE. Recently, two related formulas were proposed for this purpose. However, they have never been tested in an external population. MATERIALS AND METHODS: Consecutive patients from May 2017 to January 2018, who were admitted with the diagnosis of acute anterior STEMI, were enrolled. Electrocardiograms were systematically reviewed and only subtle ones were included. First 200 consecutive patients with noncardiac chest pain were also enrolled as a control group. Relevant electrocardiographic parameters were measured. RESULTS: A total of 379 anterior MI and 200 BV-STE cases were enrolled during study period. A total of 241 patients in STEMI group were excluded for not matching subtleness criteria, four patients in control group were also excluded because of prior left-anterior descending artery intervention. The three-variable formula, with recommended cut-point of 23.5, had a sensitivity, specificity, and diagnostic accuracy of 73.9%, 86.7%, and 81.4%, respectively. The four-variable formula, with the published cut-point of 18.2, had a sensitivity, specificity, and diagnostic accuracy of 83.3%, 87.7%, and 85.9%, respectively. CONCLUSION: Three- and four-variable formulas with recommended cutoffs have a reasonable sensitivity, specificity, and diagnostic accuracy in differentiating subtle STEMI with BV-STE. Although both perform well, the four-variable formula has a higher sensitivity, specificity, and diagnostic accuracy and should be preferred.

An algorithm for the differentiation of the infarct territory in difficult to discern electrocardiograms.

BACKGROUND: In a minority of the patients presenting with ST-segment elevation (STE) myocardial infarction (MI), electrocardiogram (ECG) may show a balanced STE in both anterior and inferior lead groups and may cause diagnostic confusion about involved myocardial territory. In this study, we sought ECG clues which may facilitate discriminating (1) MI location and then (2) culprit artery in patients with difficult-to-discern ECGs. MATERIAL AND METHODS: Consecutive patients with the diagnosis of STEMI were scanned and patients with ECGs displaying both anterior and inferior STE were enrolled. ECGs with obvious ST elevation in either lead group and reciprocal ST-segment depression were excluded. Predictive power of several ECG variables has been analyzed and an algorithm has been constructed. RESULTS: A total of 959 STEMI cases were scanned, the final study population was consisted of 114 patients. Our algorithm for locating MI territory had a sensitivity, specificity, positive and negative predictive value of 72.1%, 92.5%, 91.7% and 74.2% for inferior versus anterior location, respectively (P < 0.001, φ = 0.652). As anterior MI was strictly reserved for left anterior descending (LAD) artery occlusion, these diagnostic values were also valid for discriminating circumflex artery [Cx]/right coronary artery [RCA] versus LAD as the culprit artery. In patients classified as having inferior MI, an STE in lead III greater than STE in lead II favored RCA over Cx as the culprit artery with a sensitivity, specificity, positive and negative predictive value of 97%, 46.6%, 80% and 87.5%, respectively (P < 0.001; φ = 0.544). CONCLUSION: Our algorithm can be used in difficult-to-discern ECGs for defining involved myocardial territory and culprit artery.

[Microvascular obstruction due to thrombosis and fibrin deposition in myocardial infarction]. / Miyokart enfarktüsünde tromboz ve fibrin olusumu ile mikrovasküler tikanmanin gösterilmesi.

OBJECTIVE: It is widely known that myocardial damage is not immediately terminated after the elimination of epicardial occlusion in cases of myocardial infarction. In situ thrombosis during epicardial occlusion might contribute to poor myocardial perfusion after reperfusion of an occluded epicardial artery. In the current study, we sought to determine the effects of ischemia and reperfusion on microvascular thrombotic occlusion. METHODS: Thirty male Wistar rats were included in the study. After the rats had been anesthetized and thoracotomized, the left coronary artery was occluded for 30 minutes in the first group, and it was occluded for 30 minutes and reperfused for an additional 20 minutes in the second group. Ten rats were used as a sham-operated control group. After completion of the study protocol, excised heart preparations were analyzed by immunohistochemistry and electron microscopy. RESULTS: A significant difference was found between the infarction plus reperfusion group and the other 2 groups, with respect to microvascular fibrin and thrombocyte deposition in immunohistochemistry analysis. These results were confirmed by morphological examination with electron microscopy. CONCLUSION: In situ fibrin formation accompanies microvascular obstruction in acute myocardial infarction. Our results indicate that additional therapeutic approaches are needed in order to achieve better tissue perfusion in contemporary treatment of acute myocardial infarction after successful reopening of the infarct-related artery.

Effects of exercise on postexercise ventricular-arterial coupling and pulsatile efficiency in patients with systolic dysfunction.

BACKGROUND: A suboptimal ventricular-arterial (VA) interaction may have a prolonged depressing effect on the failing heart after functional reserves forced to their limits under stress conditions such as exercise. The continuation of excessive load in the postexercise period may be more important than the load during exercise, because the sum of postexercise periods generally exceeds exercise time itself. We sought that exercise-induced changes in postexercise VA coupling and pulsatile efficiency in patients with heart failure (HF). METHODS: Thirty consecutive HF with reduced ejection fraction (EF) and thirty age-, sex- and peak VO2 -matched subjects with preserved EF were enrolled. Pre- and postexercise echocardiographic and tonometric measurements were taken to calculate left ventricular and arterial elastances, arterial compliance and wave reflections, and steady and pulsatile power. RESULTS: VA coupling significantly deteriorated in HF group (from 1·50 ± 0·47 to 2·00 ± 0·75 mmHg/mL, P < 0·01), but control group maintained basal favourable coupling status after exercise (from 1·04 ± 0·29 to 1·03 ± 0·24 mmHg/mL, P = 0·77). Pulsatile percentage of total power significantly increased with exercise in HF group, whereas it showed a significant decrease in control group. The change in pulsatile power fraction was correlated with the change in augmentation pressure (r = 0·41, ß = 3·00, P < 0·01) and inversely correlated with the change in total arterial compliance (r = -0·29, ß = -8·52, P = 0·02). CONCLUSION: Our data indicate that exercise-induced VA decoupling and pulsatile inefficiency extend into postexercise phase in patients with systolic dysfunction. The exact duration of these derangements requires further studies.

Newly described clinical features in two siblings with MACS syndrome and a novel mutation in RIN2.

The disorder comprising Macrocephaly, Alopecia, Cutis laxa, and Scoliosis has been designated MACS syndrome. It is a rare condition, inherited in an autosomal recessive pattern. Three families from different ethnic origins have so far been reported and were all linked to homozygous mutations in RIN2, a gene encoding the Ras and Rab interactor 2 protein involved in cell trafficking. We describe herein the fourth family with MACS syndrome in two siblings carrying a novel homozygous mutation, c.1878_1879insC in exon 8 of the RIN2 gene, which predicts p.Ile627Hisfs*7. We also report on additional findings not previously described in MACS syndrome, including bronchiectasis and hypergonadotropic hypogonadism. Finally, our overall data support the argument that RIN2 syndrome is a more appropriate name for the disorder.

Is Pulmonary Capillary Wedge Pressure a Reliable Indicator of Postcapillary Pulmonary Hypertension?

Although current pulmonary hypertension (PH) guidelines recommend a pulmonary capillary wedge pressure (PCWP) >15 mm Hg for the detection of a postcapillary component, the rationale of this recommendation may not be quite compatible with the peculiar hemodynamics of PH. We hypothesize that a high PCWP alone does not necessarily indicate left-sided disease, and this diagnosis can be improved using left ventricle transmural pressure difference (∆ PTM). In this 2-center, retrospective, observational study, we enrolled 1,070 patients with PH who underwent heart catheterization, with the final study population comprising 961 cases. ∆ PTM was calculated as PCWP minus right atrial pressure. The patients with group II PH had significantly higher ∆ PTM values (12.6 ± 6.6 mm Hg) compared with the other groups (1.1 ± 4.8 in group I, 12.4 ± 6.6 in group II, 2.5 ± 6.4 in group III, and 0.8 ± 8.0 in group IV, p <0.001) despite overlapping PCWP values. A ∆ PTM cutoff of 7 mm Hg identifies left heart disease when PCWP is >15 (area under curve 0.825, 95% confidence interval 0.784 to 0.866, p <0.001). Five-year mortality was significantly higher in patients with high ∆ PTM and PCWP subgroups compared with low ∆ PTM plus high PCWP (26.1% vs 18.5%, p = 0.027) and low ∆ PTM and PCWP subgroups (26.1% vs 15.6%, p <0.001). ∆ PTM has supplementary discriminatory power in distinguishing patients with and without postcapillary PH. In conclusion, a new approach utilizing ∆ PTM may improve our understanding of PH pathophysiology and may identify a subpopulation that may potentially benefit from PH-specific treatments.

Which Diastolic Pressure Should Be Used to Assess Diastolic Function?

BACKGROUND: Although high left ventricular filling pressures [left ventricular (LV) end-diastolic pressure or pulmonary capillary wedge pressure (PCWP)] are widely taken as surrogates for LV diastolic dysfunction, the actual distending pressure that governs LV diastolic stretch is transmural pressure difference (∆PTM). Clinically, preferring ∆PTM over PCWP may improve diagnostic and therapeutic decision-making. We aimed to compare the clinical implications of diastolic function characterization based on PCWP or ∆PTM. METHODS: We retrospectively screened our hospital database for adult patients with a clinical diagnosis of heart failure who underwent right heart catheterization. Echocardiographic diastolic dysfunction was graded according to the current guidelines. LV end-diastolic properties were assessed with construction of complete end-diastolic pressure-volume relationship (EDPVR) curves using the single-beat method. Survival status was checked via the electronic national health-care system. RESULTS: A total of 693 cases were identified in our database; the final study population comprised 621 cases. ∆PTM-based, but not PCWP-based, EDPVR diastolic stiffness constants were significantly predictive of advanced diastolic dysfunction. PCWP-based diastolic stiffness constants were not able to predict 5-year mortality, whereas ∆PTM-based EDPVR stiffness constants and volumes all turned out to have significant predictive power for 5-year mortality. CONCLUSION: Left ventricular diastolic function assessment can be improved using ∆PTM instead of PCWP. As ∆PTM ultimately linked to right-sided functions, this approach emphasizes the limitations of taking LV diastolic function as an isolated phenomenon and underlines the need for a complete hemodynamic assessment involving the right heart in therapeutic and prognostic decision-making processes.

International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction.

Aims: A majority of acute coronary syndromes (ACS) present without typical ST elevation. One-third of non-ST-elevation myocardial infarction (NSTEMI) patients have an acutely occluded culprit coronary artery [occlusion myocardial infarction (OMI)], leading to poor outcomes due to delayed identification and invasive management. In this study, we sought to develop a versatile artificial intelligence (AI) model detecting acute OMI on single-standard 12-lead electrocardiograms (ECGs) and compare its performance with existing state-of-the-art diagnostic criteria. Methods and results: An AI model was developed using 18 616 ECGs from 10 543 patients with suspected ACS from an international database with clinically validated outcomes. The model was evaluated in an international cohort and compared with STEMI criteria and ECG experts in detecting OMI. The primary outcome of OMI was an acutely occluded or flow-limiting culprit artery requiring emergent revascularization. In the overall test set of 3254 ECGs from 2222 patients (age 62 ± 14 years, 67% males, 21.6% OMI), the AI model achieved an area under the curve of 0.938 [95% confidence interval (CI): 0.924-0.951] in identifying the primary OMI outcome, with superior performance [accuracy 90.9% (95% CI: 89.7-92.0), sensitivity 80.6% (95% CI: 76.8-84.0), and specificity 93.7 (95% CI: 92.6-94.8)] compared with STEMI criteria [accuracy 83.6% (95% CI: 82.1-85.1), sensitivity 32.5% (95% CI: 28.4-36.6), and specificity 97.7% (95% CI: 97.0-98.3)] and with similar performance compared with ECG experts [accuracy 90.8% (95% CI: 89.5-91.9), sensitivity 73.0% (95% CI: 68.7-77.0), and specificity 95.7% (95% CI: 94.7-96.6)]. Conclusion: The present novel ECG AI model demonstrates superior accuracy to detect acute OMI when compared with STEMI criteria. This suggests its potential to improve ACS triage, ensuring appropriate and timely referral for immediate revascularization.

Beyond the ST-segment in Occlusion Myocardial Infarction (OMI): Diagnosing the OMI-nous.

The ST-segment elevation (STE) myocardial infarction (MI)/non-STEMI (NSTEMI) paradigm has been the central dogma of emergency cardiology for the last 30 years. Although it was a major breakthrough when it was first introduced, it is now one of the most important obstacles to the further progression of modern MI care. In this article, we trace why a disease with an established underlying pathology (acute coronary occlusion [ACO]) was unintentionally labeled with a surrogate electrocardiographic sign (STEMI/NSTEMI) instead of pathologic substrate itself (ACO-MI/non-ACO-MI or occlusion MI [OMI]/non-OMI [NOMI] for short), how this fundamental mistake caused important clinical consequences, and why we should change this paradigm with a better one, namely OMI/NOMI paradigm.

Are Guideline-recommended Risk Classification Schemes in Pulmonary Hypertension Adequately Robust to Guide the Real-world Setting?

Background: Pulmonary hypertension is a complex syndrome that encompasses a diverse group of pathophysiologies predisposed by different environmental and genetic factors. It is not clear to which extent the universal risk classification schemes can be applied to cohorts in individual pulmonary hypertension centers with differing environmental backgrounds, genetic pools, referral networks. Aims: To explore whether the recommended risk classification schemes could reliably be used for mortality prediction in an unselected pulmonary hypertension population of a tertiary pulmonary hypertension center. Study Design: A retrospective cross-sectional study. Methods: We retrospectively screened our hospital database for the patients with pulmonary hypertension between 2015 and 2022. The grouping of pulmonary hypertension was made as follows in accordance with current guidelines: Group 1: patients with pulmonary arterial hypertension, Group 2: patients with pulmonary hypertension associated with left heart disease, Group 3: patients with pulmonary hypertension associated with lung disease and/or hypoxia, and Group 4: patients with pulmonary hypertension associated with pulmonary artery obstructions. Then, we compared the predicted and observed mortality rates of four different risk classification schemes (REVEAL, REVEAL-Lite, ESC/ERS and COMPERA). Results: We identified 723 cases in our pulmonary hypertension database, the final study population consisted of 549 patients. The REVEAL, REVEAL-Lite and European Society of Cardiology/European Respiratory Society risk scores significantly underestimated the mortality risk in the low-risk stratum (5.3% vs. 1.9%, P < 0.001; 5.3% vs. 2.9%, P = 0.015 and 6.3% vs. 1%, P < 0.001, respectively) and overestimated the mortality risk in the high-risk stratum (11.8% vs. 25.8%, P < 0.001; 10.4% vs. 25.1%, P < 0.001 and 13.2% vs. 30%, P < 0.001, respectively). Although the COMPERA 4-strata model significantly underestimated the risk in low- and intermediate-low risk strata (4.9% vs. 1.5%, P < 0.001 and 6.8% vs. 2.8%, P = 0.001, respectively), it was accurate in intermediate-high and high-risk groups (10.1% vs. 8.7%, P = 0.592 and 15.6% vs. 22%, P = 0.384, respectively). The analyses limited only to group 1 pulmonary hypertension patients gave similar results. Conclusion: The established risk classification schemes may not perform as good as expected in unselected pulmonary hypertension populations and this may have important implications on management decisions. Tertiary centers should not uncritically accept the published risk prediction models and consider modifying current risk scores according to their own patient characteristics.

Right Ventricular Energy Failure Predicts Mortality in Patients With Pulmonary Hypertension.

Right ventricular (RV) failure has a significant adverse impact on pulmonary hypertension (PH) prognosis. None of the currently used parameters directly assess whether RV fails to provide enough energy output to propel the blood through diseased pulmonary vascular system. Furthermore, most of the current parameters are affected by the volume status of the patient. We aimed to explore whether RV energy failure has a predictive power for mortality on top of the established prognostic risk parameters in patients with PH. We screened 723 cases from our database. A total of 3 sets of binary regression analyses were executed to determine the hazard ratios (HRs) of RV energy failure for 5-year mortality in clinical, echocardiographic, and hemodynamic context, using adjustment variables chosen according to previous studies. The final study population encompassed 549 cases. A total of 77 patients died during the 5-year follow-up (14%). RV energy failure was observed in 146 of 549 patients (26.6%). In the univariate model, RV energy failure strongly associated with increased long-term mortality (HR 4.25, 95% confidence interval [CI] 2.58 to 7.00, p <0.001). It also emerged as a significant predictor of long-term mortality in clinical and hemodynamic multivariate models (HR 2.59, 95% CI 1.43 to 4.67, p = 0.002 and HR 2.05, 95% CI 1.15 to 3.63, p = 0.015, respectively). In conclusion, our study indicates that the presence of RV energy failure independently predicts long-term mortality in PH.

Bendopnea Predicts Right Ventricular Energy Failure in Patients with Pulmonary Hypertension.

OBJECTIVE: The development of right ventricular failure has a significant adverse prognostic impact on the course of pulmonary hypertension. Right ventricular energy failure has been shown to double the mortality of pulmonary hypertension even after correction for many established risk predictors. We hypothesize that bendopnea may indicate right ventricular energy failure in patients with pulmonary hypertension. METHODS: We prospectively enrolled patients with pulmonary hypertension who were admitted to our pulmonary hypertension outpatient clinic between January 2021 and June 2021. Bendopnea was assessed by asking patients to bend forward and report any shortness of breath within 30 seconds. Routine physical examination, laboratory tests, echocardiography, and right heart catheterization parameters were collected. RESULTS: A total of 167 patients were enrolled into the study. Bendopnea and right ventricular energy failure was present in 79 (47.3%) and 43 (25.7%) patients, respectively. Bendopnea accurately predicted the presence of right ventricular energy failure (area under the curve, 0.667; 95% CI, 0.574-0.760; P < 0.001) and had a significantly superior diagnostic power compared with many other symptoms and signs. CONCLUSIONS: Our study shows that bendopnea predicts right ventricular energy failure in patients with pulmonary hypertension and can be added to our physical examination armamentarium as an easy, rapid, and noninvasive prognostic tool.

Evaluation of Pulmonary Hypertension with Exercise Right Heart Catheterization in an Adult Patient with Cor Triatriatum Sinister.

Cor triatriatum sinister (CTS) is a rare adult congenital heart disease. The usual presentation may vary according to the size of the hole in the membrane in the left atrium and the pressure gradient. In addition to acute clinical presentations including acute pulmonary edema and sudden cardiac death, patients may present with chronic findings such as right heart failure due to pulmonary hypertension. The development of pulmonary hypertension is an important indicator of mortality. In cases where non-invasive methods are not sufficient for the diagnosis of pulmonary hypertension, exercise right heart catheterization may also be used. We present a patient with CTS, in whom the final decision was made with the help of an exercise right heart catheterization.