Hypertensive acute heart failure: a critical perspective on definition, epidemiology, pathophysiology, and prognosis-a narrative review: a joint session with the Romanian Society of Cardiology (part II)

Abstract

Hypertensive acute heart failure (HT-AHF) has historically been recognized as a distinct clinical phenotype of AHF, characterized by acute pulmonary congestion in the context of elevated systolic blood pressure (SBP), typically > 140 mmHg. However, emerging evidence has begun to challenge the diagnostic accuracy, clinical utility, and relevance of this category. A main criticism of HT-AHF is its considerable overlap with other AHF clinical profiles, including acute decompensated heart failure (ADHF) and acute pulmonary oedema (APO). Clinical features such as dyspnea and pulmonary congestion are not unique to HT-AHF. Additionally, some HT-AHF patients concurrently fulfill diagnostic criteria for the ADHF phenotype, including a history of HF or signs of volume overload, leading to ambiguity in diagnosis. HT-AHF is associated with very low in-hospital mortality (0-2%) compared to other AHF phenotypes. Notably, there is no robust evidence linking high SBP to poor short- or long-term outcomes, nor are there randomized clinical trials validating distinct management strategies for HT-AHF. Often associated with the management of HT-AHF, vasodilators have shown limited benefit across trials, contributing to a downgrade in guideline recommendations. The relatively favorable short-term prognosis and the lack of a standardized, evidence-based treatment approach weaken the rationale for classifying HT-AHF as a standalone AHF category. Given the heterogeneity of clinical presentations, overlap with other AHF phenotypes, and lack of prognostic distinction or targeted therapy, the term "AHF with high SBP at presentation" offers a more flexible and clinically meaningful descriptor, encouraging a more nuanced approach to treatment.

Keywords: Definition; Hypertensive acute heart failure; Management; Systolic blood pressure.

Fig. 1

Overlapping among ADHF, HT-AHF, and APO. A. Investigator-rated classification of AHF (ref 2). Components of the definition of HT-AHF (SBP at admission>140mmHg, HTN as precipitant, HTN aetiology, EF>40%) are seen in various proportions in other clinical profiles, suggesting low accuracy of the investigator-rated classification of AHF. B. Clinical signs of pulmonary and systemic congestion can overlap between AHF clinical profiles. Although HT-AHF typically manifests with pulmonary congestion, clinical signs of systemic congestion may also be present in HT-AHF. Both APO and HT-AHF present with signs of pulmonary congestion; however, the distinction between them is primarily related to respiratory distress and respiratory failure, which are diagnostic features of APO. Abbreviations: ADHF acute decompensated heart failure; ABG arterial blood gas; APO acute pulmonary oedema; EF ejection fraction; HT-AHF hypertensive acute heart failure; JVD jugular vein distension; HJR hepatojugular reflux; RR respiratory rate; SBP systolic blood pressure; S3 sound 3

Fig. 2

Chronological structural and functional changes in longstanding HTN and association with HF stages. AHF with high SBP at admission may be present in all stages. In stages A and B, HTN determines cardiac functional abnormalities, but with a normal structural LV. Any precipitant, particularly high SBP, can lead to an HF event. Further on, uncontrolled HTN will lead to cardiac structural changes, microvascular dysfunction, and arterial stiffness. In these scenarios, HTN can be both the cause and the precipitant for “de novo” AHF. In stage C, the worsened course of symptomatic HF is the consequence of the progression from LVH to LV dilatation and may present as HFpEF or HFrEF. Various precipitants (not only high SBP) may destabilize the clinical condition and lead to worsening HF. Furthermore, as HF progresses, several cardiac (e.g. ischemia, atrial fibrillation, valvular heart diseases) and non-cardiac comorbidities (e.g. diabetes, anemia) may impact clinical worsening. Although HTN was the primary etiology in these stages, many other etiologies contribute to the pathophysiology of HF. Abbreviations: AHF acute heart failure; HTN hypertension; LV left ventricle; LVH left ventricular hypertrophy; HFpEF heart failure with preserved ejection fraction; HFrEF heart failure with reduced ejection fraction; SBP systolic blood pressure

Fig. 3

SBP response at presentation in AHF. Irrespective of the underlying etiology or type of precipitant, during AHF, enhanced neurohormonal activation favors vasoconstriction of both the arterial and venous compartments, which acutely challenges cardiac preload and afterload. This is combined with inflammatory-related leakiness of the vascular tree, most importantly the alveolar barrier, which leads to pulmonary congestion and peripheral oedema. In this milieu, the ability to increase SBP in the acute phase of HF regardless of etiology or LVEF may reflect a greater “cardiovascular reserve” that can be mediated by a greater ability to achieve a vasoconstrictive response and/or a greater myocardial contractile reserve, translating into greater cardiac output. These patients will benefit most from a vasodilator-based therapy without many diuretics because they mostly have fluid redistribution due to leakiness of blood vessels and afterload mismatch that shifts fluids to the pulmonary circulation. On the other hand, patients with low cardiac reserve usually react with low or normal SBP. Abbreviations: AHF acute heart failure; HTN hypertension; LV left ventricle; LVEDV left ventricular end-diastolic volume; LVEF left ventricular ejection fraction; NH neurohormonal activation; SBP systolic blood pressure; SVR systemic vascular resistance

Fig. 4

In AHF with high SBP at presentation, identifying different categories based on LVEF, preload, and afterload could personalize treatment. Patients with AHF and high SBP at admission may present with various combinations of alterations of preload and afterload. High preload with an increased LVEDV, due to increased venous return and reduced LV compliance, can be encountered in both HFpEF (increased LVEDP) and HFrEF patients (increased LVEDV). Drugs like diuretics and nitrates that reduce volume overload and venous return will lower preload. High SVR is likely present in AHF and very high BP, as subsequent vasoconstriction is the leading cause of high SVR. In these cases, management of high SVR decreases the LV workload, leading to high CO and better end-organ perfusion. Vasodilators such as ACE inhibitors, ARBs, calcium channel blockers, and high doses IVnitrates are the treatments of choice for reducing SVR. Use of IV diuretics in patients with high SVR and low preload is not advisable. In patients with both high preload and afterload, the treatment should be initiated with IV nitrates and then adjusted according to SBP response and evolution of congestion. Abbreviations: ACE angiotensin-converting enzyme; AHF acute heart failure; ARBs angiotensin II receptor blockers; BP blood pressure; CO cardiac output; HFpEF heart failure with preserved ejection fraction; HFrEF heart failure with reduced ejection fraction; LV left ventricle; LVEF LV ejection fraction; LVEDP LV end diastolic pressure; LVEDV LV end diastolic volume; SVR systemic vascular resistance

Fig. 5

Practical approach in patients with AHF with SBP>140 mmHg. Abbreviations: AHF acute heart failure; HJR Hepatojugular Reflux; IC Inspiratory Capacity; ISDN Isosorbide Dinitrate; IV Intravenous; mEq/L milliequivalents per Liter; IVC Inferior Vena Cava; JVD Jugular Venous Distention; NTG Nitroglycerin; RAASI Renin-angiotensin-aldosterone-system inhibitors; S3 Third Heart Sound; SBP Systolic Blood Pressure; SNP Sodium Nitroprusside