This diagnostic image shows a single-lead electrocardiogram (ECG/EKG) strip plotted on standard red grid paper, demonstrating Ventricular Fibrillation (VF). The waveform is characterized by a chaotic, irregular, and disorganized rhythm. Key morphological features include the complete absence of identifiable P waves, QRS complexes, and T waves. The tracing displays fibrillatory waves with varying amplitudes and erratic vertical deflections, indicating a lack of coordinated ventricular contraction. The amplitude of these oscillations fluctuates, generally ranging across two small grid squares relative to the isoelectric baseline. This tracing is a classic representation of a shockable cardiac arrest rhythm, emphasizing the medical importance of rapid defibrillation in Advanced Cardiovascular Life Support (ACLS) protocols. It serves as a pedagogical tool for medical students and healthcare professionals to differentiate between organized rhythms and life-threatening ventricular arrhythmias.

This diagnostic image displays a series of six representative 5-second electrocardiogram (ECG) waveform segments (labeled a-f) illustrating the progression of ventricular fibrillation (VF) over time. The segments correspond to 1, 4, 6, 8, 10, and 12 minutes post-VF induction. Initially (1 min), the waveform shows high-amplitude, coarse VF with disorganized but rapid electrical activity. From 4 to 10 minutes, there is a visible trend toward 'fine' ventricular fibrillation, characterized by a progressive decrease in both amplitude and dominant frequency as the myocardium becomes increasingly ischemic and depleted of ATP. At 10 minutes (panel e), the rhythm is near-isoelectric with very low amplitude. However, at 12 minutes (panel f), following the initiation of oxygenated blood perfusion, there is a stark morphological shift back to high-amplitude, high-frequency coarse VF. This sequence demonstrates the clinical significance of myocardial oxygenation and metabolic state in influencing VF morphology and the potential for successful defibrillation (often correlated with AMSA—Amplitude Mid-frequency Spectrum Analysis).

This diagnostic image is a continuous rhythm strip (ECG trace) illustrating ventricular fibrillation, a life-threatening cardiac arrhythmia. The waveform is characterized by rapid, chaotic, and disorganized electrical activity. There is a total absence of identifiable P waves, QRS complexes, and T waves. The baseline is highly irregular, showing undulating oscillations with variable amplitudes and frequencies, consistent with the coarse ventricular fibrillation pattern. Annotated labels 'Initial Rhythm' and 'Point 1' indicate specific chronological markers during the clinical event recorded by emergency medical services. This tracing serves as a classic educational example of a shockable cardiac arrest rhythm requiring immediate defibrillation. It highlights the loss of coordinated ventricular contraction and the resulting hemodynamic collapse associated with this arrhythmia.

Multi-panel physiological waveform series demonstrating hemodynamic changes during ventricular fibrillation (VF) and subsequent defibrillation in the context of a continuous-flow left ventricular assist device (CF-LVAD). The image consists of a grid with six time-sequenced panels (A-F) tracking four parameters: Flow rates (PF: Pump Flow in pink, PAF: Pulmonary Artery Flow in cyan), Pressures (LVP: Left Ventricular Pressure in green, AOP: Aortic Pressure in purple), Central Venous Pressure (CVP in dark blue), and Electrocardiogram (ECG in red). Panels B-E illustrate the progression of sustained VF over 60 minutes, characterized by disorganized ECG activity and a compensatory increase in CVP amplitude and baseline (rising from ~10 to 14 mmHg). During VF, LVP and AOP remain significantly depressed with low pulsatility. Panel F displays the hemodynamic recovery post-defibrillation, showing the restoration of organized QRS complexes on ECG, a return of high-amplitude rhythmic pulsatility in LVP/AOP, and a significant reduction in CVP toward a stable baseline, signifying successful conversion to sinus rhythm and restored biventricular output.

Summary : This figure presents the types and classification of Acute Coronary Syndromes, contrasting NSTEMI (Non-ST-Elevation Myocardial Infarction) and STEMI (ST-Elevation Myocardial Infarction) based on angiographic findings, electrocardiographic changes, and cardiac biomarker changes. flowchart: # Main Categories : • Acute Coronary Syndromes (central node) – Branches into: NSTEMI (left), STEMI (right) # NSTEMI : ## Angiographic Findings : • Illustration of a coronary artery with a partially occlusive thrombus. • Label: "Partially occlusive thrombus" ## Electrocardiographic Changes : • ST-segment depression (example ECG tracing) • T-wave inversion (example ECG tracing) • Note: "Nonspecific or no electrocardiographic changes may instead be seen" ## Biomarker Change (cardiac troponin) : • Unstable angina: negative (–) • NSTEMI: positive (+) # STEMI : ## Angiographic Findings : • Illustration of a coronary artery with a completely occlusive thrombus. • Label: "Completely occlusive thrombus" ## Electrocardiographic Changes : • ST-segment elevation (example ECG tracing) • Note: "ST-elevation in ≥2 contiguous leads on standard 12-lead ECG (or ST-elevation on posterior lead ECG)" ## Biomarker Change (cardiac troponin) : • Positive (+) • Note: "Might be – if short time from symptom onset" # Layout : • Two-column comparison: NSTEMI (blue background, left), STEMI (yellow background, right) • Each column subdivided into three horizontal sections: Angiographic Findings, Electrocardiographic Changes, Biomarker Change # Analysis : • NSTEMI is characterized by partial thrombus occlusion, ST-segment depression or T-wave inversion (or nonspecific ECG changes), and positive cardiac troponin. • STEMI is defined by complete thrombus occlusion, ST-segment elevation on ECG, and positive cardiac troponin (may be negative early after symptom onset). • The figure visually distinguishes the pathophysiology, ECG findings, and biomarker profiles of NSTEMI and STEMI, aiding in clinical differentiation.

A comparative diagnostic image panel illustrating differences between ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) using angiographic blush quantification and cardiac magnetic resonance (CMR). The top row (a, b) displays STEMI findings: (a) an angiographic frame with a circular red Region of Interest (ROI) showing reduced myocardial blush, and (b) a delayed-enhancement CMR image showing extensive hyperenhancement (red arrows) indicating a large transmural inferior wall infarct. The bottom row (c, d) displays NSTEMI findings: (c) an angiographic frame with higher myocardial blush density within the ROI, and (d) a delayed-enhancement CMR image showing a small, localized area of subendocardial hyperenhancement (red arrow) in the anterior wall. The visual comparison highlights the greater infarct size and transmurality associated with STEMI compared to the smaller, non-transmural nature of NSTEMI, as well as the corresponding differences in microvascular perfusion (blush) between the two clinical presentations.

Summary : This flowchart presents a revised classification of myocardial infarction (MI) based on the presence or absence of acute coronary occlusion and the underlying mechanisms, as adapted from de Lemos et al. It visually distinguishes between MI with acute coronary occlusion and MI due to oxygen supply/demand mismatch without acute coronary occlusion, further subdividing each category by specific pathophysiological causes. flowchart: # Main Categories : • Acute myocardial injury with signs and/or symptoms of ischaemia (top-level node). • Two primary branches: – MI with acute coronary occlusion. – MI due to oxygen supply/demand mismatch without acute coronary occlusion. # MI with Acute Coronary Occlusion (Left Branch) : • Plaque rupture/erosion with thrombus (circular illustration showing narrowed artery with thrombus). • Spontaneous coronary artery dissection (circular illustration showing dissection in artery wall). • Coronary embolism (circular illustration showing embolic obstruction). • Vasospasm or microvascular dysfunction (circular illustration showing narrowed vessel due to spasm). # MI Due to Oxygen Supply/Demand Mismatch Without Acute Coronary Occlusion (Right Branch) : • With fixed obstructive CAD (circular illustration showing narrowed artery with stable plaque). • Without fixed obstructive CAD (circular illustration showing normal or non-obstructed artery). # Connectors : • Downward arrows from the top node to the two main branches. • Further downward arrows from each main branch to their respective subcategories. # Layout : • Hierarchical, top-down structure. • Two main branches split horizontally, each with multiple subcategories depicted with icons/illustrations. # Technical Details : • Figure legend notes that both MI types may present with ECG changes of ST-segment elevation (STEMI) or non-ST-segment elevation (NSTEMI). • Abbreviations: CAD = coronary artery disease; MI = myocardial infarction. Analysis : • The flowchart clarifies that MI can result from either acute coronary occlusion (with several distinct mechanisms) or from an imbalance in oxygen supply and demand without acute occlusion, with or without underlying coronary artery disease. • Visual icons help differentiate the pathophysiological processes, emphasizing the heterogeneity of MI causes. • The structure supports clinical differentiation for diagnosis and management.

A multi-track genomic visualization showing the association of genetic variants at the 1p13.3 locus with myocardial infarction (MI) phenotypes. The top panel is a regional Manhattan-style plot displaying -log10(P) values for NSTEMI (red), STEMI (blue), and all MI (black) cases, distinguishing between genotyped (filled circles) and imputed (hollow triangles) variants. A gray shaded region highlights a cluster of high significance specifically for NSTEMI, with P-values reaching nearly 10^-9. Below the association plot, tracks display RefSeq genes including CD53, LRIF1, DRAM2, CEPT1, and DENND2D, alongside ENCODE regulatory annotations: Layered H3K27Ac peaks (marker of active enhancers/promoters) and DNase I hypersensitivity clusters (marker of open chromatin). The bottom track presents a Linkage Disequilibrium (LD) heat map using the D' statistic, revealing a distinct red block of high LD that corresponds spatially with the NSTEMI-associated variants and the DRAM2/CEPT1 gene region. This visual integration suggests a potential regulatory role of the identified variants in the pathogenesis of non-ST-elevation myocardial infarction.