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DOI 10.1007/s11906-014-0515-z
Introduction
Recent data suggest that systematic hypertension is the responsible cause for nearly 7.1 million deaths per year
This article is part of the Topical Collection on Hypertensive Emergencies
D. P. Papadopoulos (*) : E. A. Sanidas : N. A. Viniou :
V. Gennimata : V. Chantziara : I. Barbetseas
ESH Excellent Center of Hypertension, Department of Cardiology,
Laiko General Hospital, Athens, Greece
e-mail: jimpapdoc@yahoo.com
T. K. Makris
ESH Excellent Center of Hypertension, Elena Venizelou Maternity
Hospital, Athens, Greece
worldwide. Approximately 12 % of patients with hypertension will develop a hypertensive crisis which can be further
categorized as either hypertensive emergency or urgency depending on either the presence or absence of acute end-organ
dysfunction, respectively. Hypertensive crises can develop in
patients with or without preexisting chronic hypertension
[13] and the prevalence mirrors the distribution of essential
hypertension in the general population, with men, AfricanAmericans, and the elderly being most commonly affected
[4].
The most common cardiac emergencies associated with
severely elevated blood pressure are acute left ventricular
(LV) dysfunction with pulmonary edema (22 %), acute coronary syndromes (including acute myocardial infarctionMI)
(18 %), and aortic dissection (8 %). In the context of sympathomimetic drug abuse that can cause or mimic the above
clinical conditions, cocaine accounts for almost one third of
all visits to emergency departments [5]. Classical cardiac and
pulmonary symptoms (dyspnea, chest pain, arrhythmias, and
syncope) seem to be less common in patients presenting with
hypertensive crises (28.3 %). The majority present with nonspecific symptoms [6].
The risk of a future cardiovascular event attributable
to hypertension is greater in individuals with established
cardiovascular disease, diabetes mellitus, or chronic kidney disease compared to those without these comorbid
conditions. This increased risk led the 2003 Seventh
Joint National Committee (JNC 7) report on high blood
pressure to list heart disease, heart failure, diabetes,
chronic kidney disease, and cerebrovascular disease as
compelling indications for the treatment of hypertension. Other risk factors include peripheral artery disease
and traditional coronary risk factors such as cigarette smoking
and family history of cardiac disease [7].
Mortality rates of patients with hypertensive emergencies
has decreased significantly over the years (from 80 % in 1928
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to 10 % in 1989) [8], mainly due to the availability of antihypertensive medications. The therapeutic goal is to protect
remaining end-organ function, reduce the risk of complications, and thereby improve patient outcomes [9, 10].
The aim of this review is to summarize the current evaluation and treatment recommendations for the most common
cardiovascular clinical presentations encountered in patients
with hypertensive crisis.
Myocardial Infarction
Epidemiology Published results indicate acute MI as the
leading cause of death and hospital admission in patients with severely elevated blood pressure. Moreover,
nearly 50 % of all patients originally admitted with a
hypertensive emergency died as a result of an acute MI
during long-term follow-up. Of note, no differences
were found in regard to the presence of other cardiovascular risk factors like smoking or prevalence of
diabetes mellitus [11, 12].
Pathophysiology Hypertension is linked to MI as a risk
factor, an atherogenic factor, and a hemodynamic factor
with profound effects on morbidity and mortality. During
a hypertensive emergency, the increase in blood pressure
generates mechanical stress and endothelial injury leading
to increased permeability, activation of the coagulation
cascade and platelets, and deposition of fibrin. This process results in ischemia and release of additional vasoactive mediators generating a vicious cycle of ongoing injury. The renin-angiotensin system is often activated leading
to further vasoconstriction and production of proinflammatory cytokines such as IL-6. Furthermore, NADPH oxidase
activity is increased and generates reactive oxygen species.
These collective mechanisms can culminate in end-organ
hypoperfusion, ischemia, and dysfunction manifested as a
hypertensive emergency [13].
Clinical Presentation and Evaluation Hypertensive crisis
may lead to ischemia and MI causing angina-like chest pain.
Evaluation of cardiovascular risk factors and other comorbidities is essential. An electrocardiogram (ECG) is the gold
standard exam to reveal myocardial ischemia or infarction.
Also, vital signs should be checked carefully during the physical examination of a patient with hypertensive crisis, namely,
blood pressure, oxygen saturation, and heart rate.
Baseline laboratory analyses should be performed rapidly
after the initial evaluation of the patient. These laboratory
analyses include cardiac enzymes and a cardiac troponin-I.
In a retrospective study, patients with hypertensive crises and
elevated cardiac c-troponin-I (cTnI) had 2.7 times higher risk
for the occurrence of major adverse cardiovascular and
cerebrovascular events (MACCE) at 2 years follow-up compared to those with normal cTnI values. In patients with
hypertensive crisis, elevated cTnI confers a significantly
greater risk of long-term MACCE and is a strong predictor
of obstructive coronary artery disease [14].
Management Severe hypertension associated with an acute
MI is appropriately treated with intravenous nitroglycerin,
clevidipine, nicardipine, labetalol, or esmolol to reduce the
underlying coronary ischemia and/or increased myocardial
oxygen consumption and to improve prognosis. In addition,
reducing blood pressure improves hemodynamics, ameliorates the risk of pulmonary edema, and decreases the size of
the infarct area. If available, especially in ST-elevation MI,
primary angioplasty is the best option for reperfusion therapy
in patients with high blood pressure since thrombolysis might
increase the risk of cerebral bleeding [1518].
Nitroglycerin is a venodilator that mainly reduces the preload and decreases the cardiac oxygen demands. This agent is
primarily used in acute MI and acute pulmonary edema along
with other antihypertensive regimens [1517].
Labetalol is an alpha1 adrenergic receptor blocker and
nonselective beta-blocker. It reduces the systemic vascular
resistance, but it maintains the cerebral, renal, and coronary
blood flow. Of note, despite the beta-blocking effect, cardiac
output is maintained [1].
Esmolol is an intravenous beta1 cardioselective receptor
blocker with rapid onset and very short duration of action that
can be safely used in most patients treated for acute MI with
relative contraindications to beta-blockers. Tolerance to higher
maintenance doses of esmolol is a good predictor of subsequent outcome with oral beta-blocker therapy [19].
Other agents that can be used in hypertensive emergencies
include nicardipine (dihydropyridine calcium channel
blocker), which is a useful agent for patients with coronary
artery disease due to its beneficial effect on coronary blood
flow or clevidipine, which is a relatively new short-acting,
intravenous dihydropyridine calcium channel blocker with
non-weight-based dosing regimen, allowing prolonged infusion and successful transition to oral therapy [2022].
The optimal blood pressure after an acute coronary syndrome remains controversial. Numerous large studies have
shown an inverse relationship between diastolic pressure and
adverse cardiac ischemic events (i.e., the lower the diastolic
pressure, the greater the risk of coronary heart disease and
adverse outcomes). This effect is defined as the J-curve phenomenon which describes the shape of the relationship between blood pressure and the risk of cardiovascular morbidity
and/or mortality. The aforementioned observation appears to
be even more pronounced in patients with underlying coronary artery disease. Since coronary blood flow mainly occurs
during diastolic phase in patients with coronary heart disease,
a fall in diastolic pressure might lower perfusion pressure
distal to a stenosis below the critical level at which autoregulation is effective. Hence, reducing systolic blood pressure to
values close or below 120125 mmHg and diastolic pressure
below 7075 mmHg in patients at high cardiovascular risk
might be accompanied by an increase in the incidence of
coronary events [2325].
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Aortic Dissection
Epidemiology Aortic dissection has an estimated incidence of
3/100,000 per year. Seventy percent of these patients are
hypertensive and most of them are over 50 years of age, as
there is reduced resistance of arterial walls with age [34, 35].
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Management Antihypertensive therapy in acute aortic dissection aims specifically to lessen pulsatile load or aortic stress
(dp/dt) by lowering the blood pressure in order to retard the
propagation of the dissection and prevent aortic rupture. Pharmacological treatment aims to prevent myocardial ischemia
and decrease LV afterload and myocardial oxygen consumption. Still, only few comparative studies or randomized controlled trials provide definitive conclusions and recommendations regarding the efficacy and safety of comparative agents
[30, 38].
Hypertensive emergencies mainly require rapid blood pressure control with a parenteral antihypertensive medication
while the patient is usually admitted to the intensive care unit.
Typically, blood pressure should be reduced within minutes
to an hour approximately 2025 % and then gradually to
160/100 or 160/110 mmHg within the next 2 to 6 h. An abrupt
fall in blood pressure in patients with preexisting hypertension
may induce severe ischemic injury in major organs as a result
of the chronic adaptation of autoregulation mechanisms [20].
Unlike other hypertensive emergencies, aortic dissection is an
exception, where the rapid and immediate reduction of blood
pressure within 5 to 10 min is required. Management includes
primarily a parenteral beta-blocker. Esmolol is the drug of
choice, but labetalol, propranolol, and metoprolol can also
be used to reduce the heart rate below 60 beats per minute
and decrease the shear stress on the aortic wall. If the blood
pressure remains elevated after beta blockade administration,
a vasodilator such as nitroglycerin can be added to achieve a
systolic blood pressure of 100 to 120 mmHg (blood pressure
target: systolic blood pressure <120 mmHg and a mean
Page 5 of 6 5
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Conclusions
Cardiovascular events related to hypertensive emergencies are life-threatening situations requiring immediate
evaluation and management to prevent end-organ damage. Several regimens have proven to be effective
enough but the choice of treatment depends on the
clinical presentation of the patient. A very important
aspect of care for these patients is to assure highquality outpatient follow-up since a large proportion of
them will return to the hospital with a recurrent hypertensive emergency. Adequate control of blood pressure
should be pursued as a way to avoid this severe complication of hypertension.
Compliance with Ethics Guidelines
Conflict of Interest D.P. Papadopoulos, E.A. Sanidas, N.A. Viniou, V.
Chantziara, I. Barbetseas, and T.K. Makris declare that they have no
conflicts of interest.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
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