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.

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.

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.

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.

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.

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.

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.

Intra-aortic Balloon Occlusion for Refractory Cardiac Arrest in a Patient with Anterior Myocardial Infarction.

Despite recent advances in its management, the outcome of cardiac arrest is often poor despite appropriate cardiopulmonary resuscitation. The arteriovenous perfusion gradient achieved dur ing cardiopulmonary resuscitation is associated with the successful return of spontaneous cir culation. Continuous balloon occlusion of the descending aorta is an experimental method that can occlude the "unnecessary" part of the circulation, thus diverting generated pressure and blood flow to the heart and brain. In this study, we present a case report of a patient unre sponsive to standard cardiopulmonary resuscitation, in whom constant intra-aortic balloon occlusion achieved a return of spontaneous circulation and successful survival.

The Effects of Iron Replacement on Functional Capacity in Patients with Group 1 and Group 4 Pulmonary Hypertension.

OBJECTIVE: Abnormal iron handling complicates pulmonary hypertension (PH), causes functional limitation and poor outcomes. Although preliminary results in group 1 PH patients support the use of iron replacement, whether this applies to other PH subgroups is not known. METHODS: A total of 58 patients with an established diagnosis of group 1 or 4 PH, who had a serum ferritin of <100 ng/mL or 100 to 300 ng/mL in combination with a transferrin saturation (TSAT) <20% and received 500 to 1000 mg of ferric carboxymaltose (FCM) were included in the study. The change in ferritin levels and TSAT were calculated at 12- and 24-weeks follow-up. A six-minute walk test (6MWT) is undertaken at the first, 12-week and 24-week follow-up visits. RESULTS: In group 1 PH patients, ferritin levels increased from 14 ng/mL-1 to 133 and 90 ng/mL-1 at 12- and 24-weeks, respectively ( P < .001 for both). In group 4 PH patients, ferritin levels increased from 22.1 ng/mL-1 to 145 and 88.9 ng/mL-1 at 12- and 24-weeks, respectively ( P < .001 for both). 6MWT distances were 356, 412, and 350 m in group 1 PH patients and 260, 315 and 290 m in group 4 PH patients. Although the difference between baseline and 12-week 6MWT was significant in both groups ( P < .001 for both), this difference was lost at 24-week. CONCLUSION: Our study indicates that there is no difference in response to iron replacement in patients with group 1 and group 4 PH patients, in terms of treatment success and functional status.

The Evolution of the Cardiovascular System: A Hemodynamic Perspective.

The human cardiovascular system is a product of evolution that occurred over hundreds of thousands of years. During its long history, cardiovascular design has been shaped and reshaped by developing adaptations to the hemodynamic challenges it faced at every step. Although being momentarily beneficial for dealing with the problem they were first devised for, the evolutionary changes were built upon one another and culminated in the current scheme which may not necessarily be the ultimate or an immaculate design. Therefore, the analysis of the cardiovascular evolution provides a fascinating opportunity to spot the possible weak points of our cardiovascular system, to better understand the disease pathophysiology, and to formulate treatment alternatives. In this regard, this review tries to summarize the teleonomy of cardiovascular evolution from a hemodynamic perspective.

Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST-Segment-Elevation Myocardial Infarction (GUARD).

Background Intramyocardial edema and hemorrhage are key pathological mechanisms in the development of reperfusion-related microvascular damage in ST-segment-elevation myocardial infarction. These processes may be facilitated by abrupt restoration of intracoronary pressure and flow triggered by primary percutaneous coronary intervention. We investigated whether pressure-controlled reperfusion via gradual reopening of the infarct-related artery may limit microvascular injury in patients undergoing primary percutaneous coronary intervention. Methods and Results A total of 83 patients with ST-segment-elevation myocardial infarction were assessed for eligibility and 53 who did not meet inclusion criteria were excluded. The remaining 30 patients with totally occluded infarct-related artery were randomized to the pressure-controlled reperfusion with delayed stenting (PCRDS) group (n=15) or standard primary percutaneous coronary intervention with immediate stenting (IS) group (n=15) (intention-to-treat population). Data from 5 patients in each arm were unsuitable to be included in the final analysis. Finally, 20 patients undergoing primary percutaneous coronary intervention who were randomly assigned to either IS (n=10) or PCRDS (n=10) were included. In the PCRDS arm, a 1.5-mm balloon was used to achieve initial reperfusion with thrombolysis in myocardial infarction grade 3 flow and, subsequently, to control distal intracoronary pressure over a 30-minute monitoring period (MP) until stenting was performed. In both study groups, continuous assessment of coronary hemodynamics with intracoronary pressure and Doppler flow velocity was performed, with a final measurement of zero flow pressure (primary end point of the study) at the end of a 60-minute MP. There were no complications associated with IS or PCRDS. PCRDS effectively led to lower distal intracoronary pressures than IS over 30 minutes after reperfusion (71.2±9.37 mm Hg versus 90.13±12.09 mm Hg, P=0.001). Significant differences were noted between study arms in the microcirculatory response over MP. Microvascular perfusion progressively deteriorated in the IS group and at the end of MP, and hyperemic microvascular resistance was significantly higher in the IS arm as compared with the PCDRS arm (2.83±0.56 mm Hg.s.cm-1 versus 1.83±0.53 mm Hg.s.cm-1, P=0.001). The primary end point (zero flow pressure) was significantly lower in the PCRDS group than in the IS group (41.46±17.85 mm Hg versus 76.87±21.34 mm Hg, P=0.001). In the whole study group (n=20), reperfusion pressures measured at predefined stages in the early reperfusion period showed robust associations with zero flow pressure values measured at the end of the 1-hour MP (immediately after reperfusion: r=0.782, P<0.001; at the 10th minute: r=0.796, P<0.001; and at the 20th minute: r=0.702, P=0.001) and peak creatine kinase MB level (immediately after reperfusion: r=0.653, P=0.002; at the 10th minute: r=0.597, P=0.007; and at the 20th minute: r=0.538, P=0.017). Enzymatic myocardial infarction size was lower in the PCRDS group than in the IS group with peak troponin T (5395±2991 ng/mL versus 8874±1927 ng/mL, P=0.006) and creatine kinase MB (163.6±93.4 IU/L versus 542.2±227.4 IU/L, P<0.001). Conclusions In patients with ST-segment-elevation myocardial infarction, pressure-controlled reperfusion of the culprit vessel by means of gradual reopening of the occluded infarct-related artery (PCRDS) led to better-preserved coronary microvascular integrity and smaller myocardial infarction size, without an increase in procedural complications, compared with IS. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02732080.

Change in pulmonary arterial compliance and pulmonary pulsatile stress after balloon pulmonary angioplasty.

OBJECTIVE: Although the underlying pathology of chronic thromboembolic pulmonary hypertension (CTEPH) is mechanical obliteration of the major pulmonary vessels, high pulsatile stress penetrating into the normal distal pulmonary microvasculature resulting from reduced pulmonary arterial compliance (CPA) may cause progressive deterioration in pulmonary hemodynamics. Hypothetically, balloon pulmonary angioplasty (BPA) may be beneficial in reducing CPA and pulsatile stress in patients with CTEPH. METHODS: In total, 26 patients with available pre- and post-BPA right heart catheterization results were included in the study. BPA was performed in a series of staged procedures by 2 experienced interventional cardiologists. RESULTS: The median CPA showed a 59.2% increase (1.03 to 1.64 mL/mm Hg, p=0.005). The median pre-BPA pulsatile stress product decreased by 20.7% (4,266 to 3,380 mm Hg/min, p=0.003). A linear regression model established that the percent change in CPA after BPA accounted for 21.8% of the explained variability in the change in 6-minute walk test (p=0.009). CONCLUSION: Our results indicate that BPA decreases CPA and pulmonary pulsatile stress. These changes may be partly responsible for the improvement in functional capacity after BPA.

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.

Recognizing electrocardiographically subtle occlusion myocardial infarction and differentiating it from mimics: Ten steps to or away from cath lab.

It is increasingly evident that the ST-segment elevation (STE) myocardial infarction (MI)/non-STEMI paradigm that equates STEMI with acute coronary occlusion (ACO) is deceptive. This unfortunate paradigm, adhered to by the current guidelines, misses at least one-fourth of the ACOs, and unnecessarily over-triages a similar fraction of the patients to the catheterization laboratory. Accordingly, we have been calling for a new paradigm, the occlusion/nonocclusion MI (OMI/NOMI). Although this new OMI/NOMI paradigm is not limited to an electrocardiogram (ECG), the ECG will remain the cornerstone of this new paradigm because of its speed, repeatability, noninvasive nature, wide availability, and high diagnostic power for OMI. This review provides a step-by-step approach to ECG for the diagnosis of OMI.

Filtering electrocardiogram: Music, math, and ST-elevation myocardial infarction.

Clinicians should have a basic understanding of the working principle of the instruments they use to avoid potential pitfalls caused by post-processing of the acquired biological signals. An electrocardiogram (ECG) is no exception; many different errors can arise during the acquisition or the processing of the ECG data, which may result in dangerous misdiagnoses. We present a case where the use of an inappropriate high-pass filter led to a false diagnosis of ST-elevation myocardial infarction. In addition, this report discusses the basic mechanisms of this frequently overlooked phenomenon and methods to avoid it.