This pathophysiology diagram illustrates the anti-hypertensive mechanism of Lactiplantibacillus plantarum (Lb. plantarum) in functional foods. The process begins with Lb. plantarum fermenting milk, which produces bioactive hydrolysates. These hydrolysates function as Angiotensin-Converting Enzyme (ACE) inhibitors, targeting the zinc-binding (Zn2+) site of the ACE protein. The diagram depicts two physiological pathways influenced by this inhibition: 1) The Bradykinin Pathway: Typically, ACE degrades the vasodilator bradykinin into inactive products. By inhibiting ACE, hydrolysates prevent bradykinin degradation, promoting vasodilation and relieving hypertension. 2) The Renin-Angiotensin Pathway: Normally, ACE transforms Angiotensin I into the potent vasoconstrictor Angiotensin II, leading to vascular contraction and hypertension. The hydrolysates inhibit this transformation, preventing pathological vasoconstriction. The visual contrast emphasizes the transition from constricted, hypertensive blood vessel states to relaxed, dilated states through the modulation of enzymatic activity. This diagram serves as a model for how probiotic-derived peptides can mitigate cardiovascular risk factors by interfering with the biochemical pathways responsible for systemic blood pressure regulation.

This pathophysiology diagram illustrates the mechanism of action of imidazoline receptor agonists on blood pressure regulation. The visual is divided into a sagittal brain anatomical diagram and a secondary physiological flowchart. On the left, the diagram highlights the 'I1 imidazoline receptors' located within the Rostral Ventrolateral Medulla (RVLM) of the brainstem, situated inferior to the cerebrum and anterior to the cerebellum. Below this, three pharmacological agents—Clonidine, Moxonidine, and Rilmenidine—are listed as imidazole agonists that target these receptors. To the right, a downward flowchart depicts the systemic consequences of receptor activation: stimulation of the RVLM leads to the 'Inhibition of sympathetic nerve activity,' followed by the 'Inhibition of norepinephrine' release. This progression results in 'Decreased vasoconstriction,' visually represented by an illustration of a dilated blood vessel with reduced smooth muscle tension. The final clinical outcome is identified as 'Reduced blood pressure.' The content is designed for intermediate medical education, focusing on neuropharmacology and cardiovascular physiology.

A medical infographic and pathophysiology diagram summarizing the long-term impact of COVID-19 on blood pressure based on a retrospective cohort study. The upper portion illustrates the cellular mechanism where SARS-CoV-2 leads to the downregulation of ACE-2 receptors, causing RAAS dysregulation (increased Ang II binding to AT1R and decreased Ang 1-7 binding to Mas receptors), endothelial dysfunction, and inflammation. The left panel details the 'Settings and participants' section, noting a study of 5,355 eligible patients with documented BP pre- and post-infection. The central 'BP change' panel shows quantitative increases in systolic blood pressure (SBP from 126.90 to 136.99 mmHg) and diastolic blood pressure (DBP from 80.54 to 86.49 mmHg), highlighted with red upward arrows. The right panel lists clinical predictors of BP changes, including smoking, diabetes, cardiovascular events, hypertension, and age, accompanied by illustrative icons. The graphic integrates clinical data with biological mechanisms to demonstrate the cardiovascular sequelae of COVID-19.

A pathophysiology diagram titled 'Impact of hypertension on viral immunity' comparing cellular immune responses under normal and hypertensive conditions. The top panel, 'Normal blood pressure,' illustrates a dendritic cell presenting antigens to a T cell via receptor-ligand interactions and cytokine release. This stimulation leads to robust T-cell activation and proliferation, resulting in a large cluster of effector T cells essential for viral clearance. The bottom panel, 'Hypertension,' depicts the same initial dendritic cell-T cell interaction but highlights the presence of elevated Angiotensin II. Angiotensin II binds to Angiotensin II receptors expressed on the activated T cell. This signaling inhibits sustained proliferation and instead promotes a T-cell contraction phase, resulting in a significantly reduced population of T cells. The diagram indicates that this hypertensive state leads to an impaired effector response and delayed viral clearance. Key components labeled include dendritic cells, T cells, cytokines, Angiotensin II, and Angiotensin II receptors.

Recommendation Table 9 — Recommendations for assessing cardiac hypertension-mediated organ damage <table><thead><tr><th>Recommendation</th><th>Class^a</th><th>Level^b</th></tr></thead><tbody><tr><td>A 12-lead ECG is recommended for all patients with hypertension.^31,281</td><td>I</td><td>B</td></tr></tbody></table>

Summary : This figure provides a structured overview of how to measure and diagnose hypertension-mediated organ damage (HMOD) in the kidney, heart, and arteries, including what to measure, diagnostic criteria, and clinical indications for assessment. flowchart/table hybrid: # Why measure? : • Support decision to start or intensify blood pressure (BP)-lowering treatment for: – Individuals with elevated BP and SCORE2/SCORE2-OP risk of 5–<10% – Uncertain situations (BP/risk close to thresholds, masked/white-coat hypertension, non-traditional CVD risk factors) – Individuals <40 years old with elevated BP – Assistance overcoming patient/physician inertia # Which organ? : • Kidney • Heart • Arteries # What to measure? : ## Kidney : • eGFR (estimated glomerular filtration rate) • ACR (albumin-to-creatinine ratio) ## Heart : • ECG • Echocardiography • Cardiac biomarkers ## Arteries : • Carotid or femoral ultrasound • Pulse wave velocity • Cardiac CT # How to diagnose HMOD? : ## Kidney : • Moderate-to-severe kidney disease: – eGFR <60 mL/min/1.73 m² (irrespective of albuminuria) – Albuminuria ≥30 mg/g (irrespective of eGFR) ## Heart : • LVH (left ventricular hypertrophy) by ECG: – Sokolow–Lyon: SV1+RV5 >35 mm – RaVL ≥11 mm – Cornell voltage: SV3+RaVL >28 mm (men), >20 mm (women) • LVH by echocardiography: – LV mass/height².⁷ (g/m².⁷): >50 (men), >47 (women) – LV mass/BSA (g/m²): >115 (men), >95 (women) – LV concentric geometry: RWT ≥0.43 • Diastolic dysfunction: – LA volume/height² (mL/m²): >18.5 (men), >16.5 (women) – LA volume index (mL/m²): 34 – e’ <7cm; E/e’ >14 • Cardiac biomarkers: – hs-cTnT or >99th percentile upper reference limit – NT-proBNP >125 pg/mL (<75 years) or >450 pg/mL (≥75 years) ## Arteries : • Carotid/femoral ultrasound: Plaque (focal wall thickening >1.5 mm) • Pulse wave velocity: – Carotid-femoral PWV >10 m/s – Brachial-ankle PWV >14 m/s • Cardiac CT: Coronary artery calcium score >100 Agatston units # Design Encodings : • Organ sections are colour-coded: kidney (purple), heart (light purple), arteries (blue). • Icons represent each organ and measurement modality. • Diagnostic criteria are listed in shaded boxes for each organ. # Layout : • Four main columns: Why measure?, Which organ?, What to measure?, How to diagnose HMOD? • Rows for kidney, heart, and arteries, each with corresponding measurements and criteria. # Analysis : • The figure provides a comprehensive, organ-based approach to diagnosing HMOD, with clear measurement modalities and diagnostic thresholds for kidney, heart, and arterial damage. • It highlights the importance of tailored assessment based on clinical context and risk, and provides actionable criteria for each organ system. • The use of colour and icons aids rapid identification of organ systems and measurement types.

A standard 12-lead electrocardiogram (ECG) demonstrating several diagnostic abnormalities relevant to cardiovascular pathology. The tracing shows a rhythm characterized as ectopic atrial rhythm with visible atrial premature complexes (APCs). Voltage criteria for left ventricular hypertrophy (LVH) are met, notably evidenced by deep S waves in the right precordial leads (V1-V3) and tall R waves in the left precordial leads (V4-V6). Associated secondary repolarization abnormalities are present, including ST-segment elevation in the anterior leads (V1-V3) and T-wave inversions in the lateral leads, which are commonly associated with LVH-related strain patterns. The PR interval appears borderline prolonged, and the QTc is noted as 470 ms. This diagnostic image illustrates the electrical manifestations of structural heart disease, specifically left ventricular hypertrophy and atrial ectopy, in a clinical context of secondary hypertension and end-stage renal disease.

Summary : This figure presents a clinical guideline recommendation for first-line antihypertensive drug therapy in adults, including the class of recommendation (COR) and level of evidence (LOE). table: COR & LOE : • COR: 1 (Class of Recommendation 1, indicating strong recommendation). • LOE: A (Level of Evidence A, indicating high-quality evidence). Recommendation : • For adults initiating antihypertensive drug therapy, the following are recommended as first-line therapy to prevent cardiovascular disease (CVD): – Thiazide-type diuretics – Long-acting dihydropyridine calcium channel blockers (CCB) – Angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB) • Recommendation is supported by references 1 and 2. Analysis : • The figure provides a clear, evidence-based recommendation for initial antihypertensive therapy, prioritizing specific drug classes based on strong evidence for CVD prevention. • The use of COR 1 and LOE A signals that these recommendations are both strongly endorsed and supported by robust clinical data.

Summary : This flowchart presents the ASCVD (Atherosclerotic Cardiovascular Disease) risk reduction algorithm for hypertension management, outlining stepwise goals, interventions, and medication options. flowchart: # Nodes : • GOAL: <130 SYSTOLIC/<80 DIASTOLIC mmHg (rectangle, blue) • LIFESTYLE INTERVENTION: Decrease Sodium Intake | Diet (DASH, Mediterranean) | Physical Activity | Achieve Optimal Weight (rectangle, blue) • ARB OR ACE: For initial blood pressure >150/100 mmHg, consider starting DUAL THERAPY combined with another agent below (rectangle, purple) • TITRATE MEDICATION DOSE OR ADD ON THERAPY EVERY 2-3 MONTHS TO REACH GOAL (rectangle, orange) • THIAZIDE | CALCIUM CHANNEL BLOCKER (rectangle, blue) • COMBINED α-β BLOCKER | β1 SELECTIVE BLOCKER | MINERALOCORTICOID RA (rectangle, orange) • ADDITIONAL ANTIHYPERTENSIVE AGENTS: CENTRAL α2 AGONIST | PERIPHERAL α1-BLOCKER | HYDRALAZINE (rectangle, red) # Connectors : • Top-down linear flow from goal setting, lifestyle intervention, initial medication choice, titration, and escalation to additional agents. • ARB/ACE node includes a branch for dual therapy if initial BP is >150/100 mmHg. • Medication escalation proceeds in order: thiazide/calcium channel blocker → combined blockers/mineralocorticoid RA → additional antihypertensive agents. # Layout : • Vertically stacked rectangles, each representing a step in the algorithm. • Colour-coded sections: blue for goals/lifestyle/first-line agents, purple for ARB/ACE, orange for titration/combination, red for additional agents. • Footnotes and references are included at the bottom for clinical context and special considerations. # Analysis : • The algorithm emphasizes a stepwise approach: starting with lifestyle changes, then progressing to medication based on blood pressure severity and response. • Dual therapy is recommended for very high initial BP (>150/100 mmHg). • Medication titration and escalation are structured, with clear options for combination and additional agents. • Colour coding visually separates intervention types and escalation steps. • The flowchart provides a comprehensive, guideline-based pathway for hypertension management in ASCVD risk reduction.

Recommendation Table 16 — Recommendations for pharmacological treatment of hypertension (see Evidence Tables 27, 28, and 29) <table><thead><tr><th>Recommendations</th><th>Class^a</th><th>Level^b</th></tr></thead><tbody><tr><td>Among all BP-lowering drugs, ACE inhibitors, ARBs, dihydropyridine CCBs, and diuretics (thiazides and thiazide-like drugs such as chlorthalidone and indapamide) have demonstrated the most effective reduction of BP and CVD events, and are therefore recommended as first-line treatments to lower BP.^122,446</td><td>I</td><td>A</td></tr><tr><td>It is recommended that beta-blockers are combined with any of the other major BP-lowering drug classes when there are other compelling indications for their use, e.g. angina, post-myocardial infarction, heart failure with reduced ejection fraction, or for heart rate control.^122,448-450</td><td>I</td><td>A</td></tr><tr><td>It is recommended to take medications at the most convenient time of day for the patient to establish a habitual pattern of medication taking to improve adherence.^246,513</td><td>I</td><td>B</td></tr><tr><td>Given trial evidence for more effective BP control vs. monotherapy, combination BP-lowering treatment is recommended for most patients with confirmed hypertension (BP ≥140/90 mmHg) as initial therapy. Preferred combinations are a RAS blocker (either an ACE inhibitor or an ARB) with a dihydropyridine CCB or diuretic. Exceptions to consider include patients aged ≥85 years, those with symptomatic orthostatic hypotension, moderate-to-severe frailty, or elevated BP (systolic BP 120–139 mmHg or diastolic BP 70–89 mmHg) with a concomitant indication for treatment.^{131,480,483,484,489}</td><td>I</td><td>B</td></tr></tbody></table>