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effective therapies for controlling the ventricular rate. However, chronic
therapy of an ectopic AT often involves the use of an antiarrhythmic agent
and/or catheter ablation. The choice of antiarrhythmic varies with the clinical characteristics of the patient and may include amiodarone, sotalol or
agents such as flecainide or propafenone. Depending on the location of
the ectopic focus and the experience of the operator, the success rates for
ablation approach 80%–85%.
3
Ventricular Arrhythmias
The definition of sustained ventricular tachycardia (VT) is a ventricular
rhythm at a rate of ≥100 bpm lasting at least 30 s in duration. VTs are categorized as occurring in the setting of structural heart disease and in the
“normal heart.” It is important to identify whether structural heart disease
is present in the patient with VT, as the treatments offered may be very
different. Structural heart disease is most commonly the result of coronary
artery disease and prior myocardial infarction; however, VT may also
occur in the setting of a nonischemic cardiomyopathy. In addition, it is
critical to differentiate between the occurrence of monomorphic VT and
of polymorphic VT or ventricular fibrillation. Over the last several years,
there have been a number of genetic conditions, such as the long QT syndromes (LQTSs), Brugada syndrome and catecholaminergic polymorphic
254
A. Fischer
Fig. 4. Telemetry recording of a run of atrial ectopic beats. The arrow indicates the
first atrial ectopic beat with a P wave morphology different from that present in sinus
rhythm.
VT (CPVT), that occur in younger patients with a structurally normal
heart. The VT seen in these patients is polymorphic rather than monomorphic and these patients constitute a unique population of patients, each
with a specific treatment approach beyond the scope of this chapter.
Ventricular Tachycardia in the Absence of Structural Heart Disease (Idiopathic VT)
It is important to understand that monomorphic VT which occurs in the setting of a structurally normal heart carries a good prognosis. The VTs occurring in these patients can be subdivided into those with a left bundle branch
block (LBBB) morphology and those with a right bundle branch (RBBB)
morphology. In general, VTs with an LBBB morphology arise from the
right ventricle (RV) and those with an RBBB, from the left ventricle (LV).
Left bundle branch block VT
The most common anatomic location of an LBBB morphology VT is the
right-ventricular outflow tract (RVOT). The typical ECG of this VT has
an LBBB morphology with an inferior axis and characteristic upright
QRS complexes in the inferior limb leads (Fig. 5). This VT often occurs
in young patients, is often provoked by exercise and frequently is repetitive. As mentioned previously, this form of VT is not associated with
increased mortality or risk of sudden death. Patients can be treated pharmacologically, as this arrhythmia is often responsive to beta-blockers, calcium channel blockers, adenosine and vagal maneuvers. Induction of this
VT by programmed electrical stimulation may be difficult and specific
maneuvers in the EP laboratory are often required for provocation. Radio
frequency ablation of the VT focus can be performed as a curative therapy, with the success rates of ablation being 90%–95%.
4
Right bundle branch block VT
A less common form of idiopathic VT, also associated with an excellent
long-term and low risk of sudden death, involves the Purkinje tissue in the
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Arrhythmias: Supraventricular, Ventricular Tachycardias and Bradyarrhythmias
LV. This form of VT is often paroxysmal and is less likely to be induced
by exercise. Induction of this arrhythmia in the EP laboratory occurs in
almost 90% of cases (as opposed to LBBB VT). Classically, this form of
VT is responsive to verapamil but other antiarrhythmic agents, specifically class III antiarrhythmics, are often used. Catheter ablation for this
form of VT is highly successful.
Ventricular Tachycardia in the Presence of Structural Heart Disease
Ischemic cardiomyopathy
The most common setting for VT in patients with coronary artery disease
(CAD) is postmyocardial infarction. Patients who present with VT in the
setting of CAD and myocardial infarction (MI) often have a significant
reduction in left-ventricular function, which is a significant predictor of
long-term mortality in these patients. The presence of myocardial scarring and fibrosis as a result of MI acts as the substrate for re-entrant
256
A. Fischer
Fig. 5. Twelve-lead electrocardiogram of right-ventricular outflow tract (RVOT) VT.
The QRS morphology in lead V1 has a left bundle branch (LBBB) morphology and the
QRS is upright in leads II, III, aVF is inferior.
ventricular arrhythmias. There have been numerous large multicenter trials that have positioned the implantable cardioverter defibrillator (ICD)
as the first-line therapy for patients with CAD and a reduced ejection
fraction of ≤35%, even in the absence of VT.
5
Based on the results of
these trials and the overwhelming evidence that these devices significantly reduce the incidence of sudden death, these devices are implanted
for primary prevention in select patients.
In addition to the use of ICDs, antiarrhythmic drugs can be employed
in the patient with VT in the setting of ischemic heart disease to suppress
recurrent VT. Often antiarrhythmics are initiated in response to ICD
shocks, but radio frequency ablation of the VT substrate is being performed more commonly as a means of reducing ICD therapies in patients
with recurrent VT. Re-entrant VT in the setting of an ischemic cardiomyopathy is often easily and reproducibly induced in the EP laboratory, allowing for mapping of the precise location of the substrate of the
VT. The success rates for ablation of VT show that it is often a more
definitive therapy that reduces the need for long-term antiarrhythmic
medications.
Nonischemic cardiomyopathy
Left-ventricular function is an important determinant of mortality in
patients with a nonischemic cause of cardiomyopathy. The presence of
asymptomatic nonsustained VT is almost universal in patients with nonischemic cardiomyopathy, with the incidence increasing as the New York
Heart Association (NYHA) functional class worsens. As is the case with
ischemic cardiomyopathy, ICD therapy is the first-line treatment for
patients with nonischemic cardiomyopathy and an LV ejection fraction of
≤ 35%, even in the absence of VT.
5
Data from large randomized trials
have demonstrated the mortality benefit of primary prevention ICD
implantation in this patient population. It is important to rule out
reversible causes of cardiomyopathy in the nonischemic patient prior to
implanting a permanent device. The approach to treating recurrent VT in
the nonischemic patient is similar to that in the patient with ischemic
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Arrhythmias: Supraventricular, Ventricular Tachycardias and Bradyarrhythmias
cardiomyopathy. Often antiarrhythmics are used as first-line therapy, but
ablation is becoming a more widely accepted approach to treating VT in
these patients.
References
1. Clague JR, et al. (2001) Targeting the slow pathway for atrioventric-
ular nodal re*entrant tachycardia: Initial results and long-term followup in 379 consecutive patients. Eur Heart J 22: 82–88.
2. Lee PC, et al. (2006) Electrophysiologic characteristics and radiofre-
quency catheter ablation in children with Wolff–Parkinson–White
syndrome. Pacing Clin Electrophysiol 29: 490–495.
3. Hsieh MH, Chen SA. Catheter ablation of focal atrial tachycardia. In:
Zipes DP, Haissaguerre M, (eds). Catheter Ablation of Arrhythmias
2nd ed. Futura, Armonk, New York, pp. 185–203.
4. Joshi S, Wilber DJ. (2005) Ablation of idiopathic right ventricular
outflow tract tachycardia: Current perspectives. J Cardiovasc
Electrophysiol 16(Suppl 1): S52–S58.
5. Bardy GH, et al. (2005) Amiodarone or an implantable cardioverter-
defibrillator for congestive heart failure. N Engl J Med 352: 225–237.
258
A. Fischer
Malignant Hypertension
Adam Harris* and Michael C. Kim
†
Key Pearls
• Severely elevated blood pressure with evidence of end organ damage
is a hypertensive emergency; medications should be administered
parenterally and pressures should be reduced by 25% within the first
4 hours.
• Symptoms occur acutely, as the result of several positive feedback
mechanisms that contribute to a rapid rise in blood pressures.
• A wide variety of clinical presentations are possible based on
underlying disease states, including hypertensive encephalopathy, MI,
aortic dissection, renal failure, vision disruptions and salt imbalances.
• Hypertensive encephalopathy is very common in patients with malig-
nant hypertension but is a rapidly reversible condition if treated in a
timely fashion; neurological symptoms include headache, nausea,
vision loss, projectile vomiting, restlessness, confusion, drowsiness
and seizures.
• Treatment options differ based on underlying organ damage and thus
it is critical to discern these conditions rapidly through physical exam,
radiology and laboratory testing.
259
*Stony Brook School of Medicine, Stony Brook, NY, USA.
†
Mount Sinai Medical Center, New York, NY, USA.
24
Chapter
Introduction
Malignant hypertension (also known as accelerated hypertension) is
defined as severely elevated blood pressure (BP) (>180/120 mmHg) associated with papilledema. In situations where there is evidence of organ
failure, it is considered a hypertensive emergency and a rapid reduction in
BP is required to minimize damage. However, if the patient presents with
severely elevated BP, but no acute end organ damage, it is considered a
hypertensive urgency and BP can be reduced more slowly.
2,7
Incidence and Etiology
Malignant hypertension occurs in approximately 1% of the hypertensive
population. It could develop de novo but this is unlikely.
9,11
Although
patients with secondary hypertension account for only 5% of the hypertensive population, they represent up to 40% of patients who present with
malignant hypertension.
8
sion, and others who were previously normotensive, develop organ damage at lower BPs and earlier in the course of their hypertensive conditions
when compared to patients with underlying chronic hypertension who
have developed adaptations to withstand higher pressures.
3
Thus, the
onset of malignant hypertension is more correlated with the rate at which
BP changes than any absolute BP.
1–3
(Table 1)
Pathophysiology
Hypertensive emergencies are the result of rapid intense systemic vasoconstriction with profound volume depletion.
1,10
Severely elevated BP exceeds
the vascular autoregulatory ability to protect microvasculature. When this
occurs, several positive feedback mechanisms are set off exacerbating
already high pressures, thus symptoms manifest very rapidly (Fig. 1).
Under conditions of extreme hypertension, autoregulation, which normally protects vascular endothelium from elevations in BP through vasoconstriction, is no longer able to compensate. High pressures are
260
A.Harris and M. Kim
transmitted to microvasculature, leading to endothelial damage and fibrinoid necrosis with intimal proliferation. These changes lead to luminal
narrowing, increasing peripheral resistance.
9
In the kidney the transmis-
sion of such pressure to capillary beds results in pressure natriuresis and
261
Malignant Hypertension
Table. 1.
1,7
Causes of Hypertensive Emergencies
• Essential hypertension (most common)
• Renal disease
Chronic pyelonephritis
Primary glomerulonephritis
Vasculitis
Microscopic polyarteritis nodosa
Wegner’s granulomatosis
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Systemic sclerosis
Systemic lupus erythematosus
• Renovascular disease
Renal artery stenosis (atheromatous or fibromuscular dysplasia)
Polyarteritis nodosa
• Pregnancy
Severe pre-eclampsia/eclampsia
• Endocrine
Pheochromocytoma
Cushing’s syndrome
Renin-secreting tumors
Primary hyperaldosteronism
• Drugs
Cocaine or other sympathomimetics
Erythropoietin
Cyclosporin
Abrupt withdrawal of centrally acting α2-adrenergic agonist
Interactions with nonselective monoamine-oxidase inhibitors
• Central-nervous-system disorders
Head injury
Cerebral infarction/hemorrhage
Brain tumors
subsequent volume depletion. The resulting hypovolemia further induces
systemic vasoconstriction as well as activates the rennin–angiotensin–
aldosterone system (RAAS). Angiotensin activation causes vasoconstriction and stimulates aldosterone secretion, leading to salt retention,
elevating BPs and possibly resulting in cardiac complications.
3
Lastly, for
reasons which are not entirely clear, under conditions of extreme pressure,
endothelial vasodilitory function is lost.
1
Clinical Presentation
Patients presenting with malignant hypertension can have diastolic
pressures that range from 100 to 180 mmHg and systolic pressures from
150 to 290 mmHg. Other clinical manifestations of malignant
262
A.Harris and M. Kim
Fig. 1.7Pathophysiology of malignant hypertension.
hypertension are highly variable depending on underlying hypertensive
conditions and its effects on particular organ systems. Generalized presentation includes weakness and malaise. Weight loss and salt imbalances
are often the result of volume depletion.
2
Ophthalmic Manifestations
35%–60% of patients presenting with malignant hypertension complain of
vision loss, likely the result of papilledema — optic disk swelling resulting
from high intracranial pressure.
2,10
Other ophthalmic changes include cot-
ton-wool spots, flame hemorrhages and the presence of a macula star.
Neurological Changes (Hypertensive Encephalopathy)
Acute hypertensive encephalopathy is common in patients presenting
with malignant hypertension. More than 60% present with headaches and
30% complain of dizziness.
2
Other neurological symptoms include nausea,
projectile vomiting, restlessness, confusion, drowsiness and seizure.
Hypertensive encephalopathy is believed to be the result of a “breakthrough” of cerebral autoregulation. This results in an interruption of the
blood–brain barrier and consequently cerebral edema along with local
changes in ionic and neurotransmitter concentrations, which leads to
neurological impairments.
10
Cardiovascular Complications
Heart failure leading to pulmonary edema is present in about 11% of
patients. The abrupt rise in BP dramatically increases cardiac wall stress,
which results in elevated oxygen demand, leading to myocardial ischemia
and possible infarct, particularly in patients with underlying coronary
artery disease. In addition, secondary hyperaldosteronism may result in
hypokalemia and associated cardiac abnormalities. Finally, although
uncommon, aortic dissection is also a possibility and represents the most
rapidly fatal complication.
1,2
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Malignant Hypertension