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European Journal of Heart Failure 2002 4(5):655-660; doi:10.1016/S1388-9842(02)00160-5
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© 2002 European Society of Cardiology

Hypertensive crisis and acute, reversible, left ventricular systolic dysfunction: a case report

Antonio D'Aloia, Claudia Fiorina, Enrico Vizzardi, Pompilio Faggiano* and Livio Dei Cas

Chair of Cardiology, University of Brescia and Cardiology Division Spedali Civili, Brescia, Italy

* Corresponding author. Via S. Antonio, 6 25133 Brescia, Italy. Tel.: +39-030-2007785; fax: +39-030-2007785. E-mail address: faggiano{at}numerica.it

Key Words: Left ventricular systolic dysfunction • Acute pulmonary oedema • Systemic hypertension • Hypertensive emergencies

Received September 14, 2001; Revised December 5, 2001; Accepted May 29, 2002


   1. Introduction
Top
 1. Introduction
2. Case report
 3. Discussion
 References
 
High blood pressure and left ventricular hypertrophy are powerful, independent predictors of heart failure [1,2]. Hypertensive emergencies are usually life-threatening situations caused by acute and marked blood-pressure elevation. Such emergencies include isolated hypertensive crisis, left ventricular heart failure, intracranial bleeding and renal insufficiency [3].

Most patients with acute pulmonary oedema due to systemic hypertension have normal left-ventricular ejection fraction. In these situations, acute heart failure has been attributed to left ventricular diastolic dysfunction [4,5]. However, pulmonary oedema may also be due to transient left ventricular systolic dysfunction associated with mitral regurgitation or acute myocardial ischemia.

We describe a patient affected by a severe and prolonged increase in arterial blood pressure, associated with acute pulmonary oedema, concomitant severe left ventricular dilatation and systolic dysfunction, which were completely normalised after a few days of intensive medical treatment. We speculate on the pathogenesis of acute pulmonary oedema and left ventricular systolic dysfunction due to hypertensive crisis.


   2. Case report
Top
 1. Introduction
 2. Case report
3. Discussion
 References
 
A 29-year-old man, slightly overweight (100 kg; 185 cm in height; body mass index, 29), without significant past medical history or cardiovascular risk factors, was admitted to our department with severe dyspnoea and generalised malaise over the previous few weeks. The patient had no family history of cardiovascular disease, was a non-smoker, did not drink alcohol and did not take any medication. Furthermore, he was totally asymptomatic, with persistently normal arterial blood-pressure values prior to the current clinical picture. Approximately 20 days prior to hospital admission, he had experienced an episode of breathlessness and coughing, initially thought to be due to bronchitis, which was empirically treated with antibiotics for 1 week. Pulmonary evaluation excluded any other underlying pulmonary disease. Over the following days, he continued to complain of exertional dyspnoea, which progressed to resting dyspnoea in the 2 days prior to hospital admission.

A chest X-ray performed prior to hospital admission showed severe enlargement of the cardiac profile, pulmonary congestion and oedema; accordingly, the patient was urgently admitted to our intensive care unit.

On admission, the patient was awake and communicative, but agitated; he complained of intense dyspnoea and was coughing without expectoration. On physical examination, he was diaphoretic and dyspnoeic. Vital signs were: polypnea (28 breaths/min), very high systemic blood pressure (270/170 mmHg) and tachycardia (140 beats/min). Transient mydriasis was observed, but neurological examination was negative. A fundoscopic examination revealed only mild signs of retinopathy.

On cardiac auscultation, gallop sound and T3 were present with bilateral fine rales at pulmonary lower and medium fields. Peripheral pulses were normal.

Laboratory test results revealed transient, mild leukocytosis (13 600 /mm3) and lymphocytopenia, which spontaneously resolved after 12 h. Blood urea and creatinine levels were slightly elevated (60 and 1.4 mg/dl, respectively) and increased to 80 and 2.0 mg/dl, respectively, over the next few days. All other parameters were within the normal limits, although LDH was mildly elevated (687 U/l) and spontaneous protrombin time (PT) was 70%, but liver function was normal.

Blood gas analysis on air was: pH 7.46, pO2, 85 mmHg; pCO2, 30 mmHg; HCO3, 23 mEq/l; and saturated O2, 85%.

Urinalysis showed blood 3+, proteins 3+ and granular/hyaline casts, with crystal oxalate.

Viral antibody titres, antinuclear antibodies, tumour markers, catecholamines, vanillylmandelic acid, ACTH, cortisol, aldosterone, thyroid and rheumatic tests were all normal.

C-reactive protein was 4.3 mg/l, rheumatoid factor was <9.9 IU/ml, renin activity was 7.6 ng/ml h in orthostatism (normal range 1.5–5.6) and 5.6 ng/ml h in clinostatism (normal range 0.2–2.7) before treatment.

Electrocardiogram (ECG) on admission showed sinus tachycardia, signs of left atrial enlargement, left ventricular hypertrophy and overload (Fig. 1a).


Figure 1
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  		Fig. 1 Electrocardiograms taken: (a) on admission with acute pulmonary oedema; and (b) 7 and (c) 15 days after antihypertensive treatment and clinical improvement. The electrocardiographic signs of left ventricular hypertrophy and strain observed an entry gradually disappeared over the following days.

 
A chest X-ray confirmed marked enlargement of the left ventricular profile and enlargement of the proximal vascular tree; the cardiothoracic ratio was 0.62. Pulmonary congestion was evident, but there were no signs of inflammatory processes (Fig. 2a).


Figure 2
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  		Fig. 2 Chest X-rays (a) on presentation with acute pulmonary oedema and (b) after 15 days of antihypertensive treatment with clinical improvement. Radiographic signs of cardiac enlargement and pulmonary congestion, which were present on admission, were normalised after 2 weeks.

 
Two-dimensional transthoracic echocardiographic examination with colour Doppler study showed a dilated left atrium (50 mm) and left ventricle (end-diastolic diameter, 70 mm; end-systolic diameter, 49 mm) with severe and diffuse hypokinesis. Left ventricular ejection fraction was approximately 15%. Left ventricular wall thickness was mildly increased (interventricular septum, 13 mm); a mild-to-moderate mitral regurgitation was detected, with Doppler signs of increased left ventricular filling pressure (restrictive pattern of transmitral blood flow). The right chambers were also dilated, with tricuspid regurgitation and Doppler signs of pulmonary hypertension (Table 1).


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  		Table 1 Comparison of echocardiographic data at baseline and after 20 days of treatment

 
Left ventricular ejection fraction measured by cardiac gated blood-pool scan (Muga) shortly after admission was 20% (Fig. 3a). Concomitant pulmonary embolism was excluded by pulmonary perfusion scintography. Coronary angiography for ischemic heart disease was negative.


Figure 3
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  		Fig. 3 Radionuclide angiography obtained (a) after a few days of acute pulmonary oedema and (b) after 20 days of antihypertensive treatment. Left ventricular ejection fraction increased from 20 to 65%.

 
The patient had no history of administration of exogenous substances (non-steroidal anti-inflammatory drugs, anabolic steroids, alcohol or tricyclic antidepressants). Since hypertensive emergencies in young people are usually due to secondary causes of hypertension, a careful differential diagnosis was performed. Renal ultrasound was unremarkable and showed no evidence of renal stenosis, and sequential kidney scan showed normal bilateral perfusion. Endocrinological work-up was negative for phaeochromocytoma, multiple endocrine neoplasia or thyroid disease. Immunological screening was also negative.

Finally, computed tomography (CT) pelvic–abdominal scan and total-body nuclear scan by 123I MIBG were performed and the results were negative.

The patient was started on oxygen and antihypertensive therapy, with intravenous sodium nitroprusside for approximately 10 days (doses were modulated to obtain an adequate blood pressure reduction), furosemide at 40 mg/day and dopamine at renal dosage (1–2 µg/kg min). The pulmonary oedema resolved in 2 days without any other respiratory difficulties. However, the patient continued to have episodes of elevated blood pressure, with values as high as 210/110 mmHg despite high doses of nitroprusside. Eventually, the blood pressure started to decrease after 5–6 days of oral antihypertensive therapy, including an ACE inhibitor (enalapril 10 mg/bid), angiotensin II antagonist (irbersartan 150 mg/bid), calcium channel blocker (amlodipine 20 mg/bid), beta-blocker (carvedilol gradually increased to 25 mg/tid), transdermal clonidine 5 mg and oral/sublingual nitrate (40 mg/bid). The patient's clinical status gradually improved, resting symptoms disappeared and a progressive increase in exercise tolerance was observed.

Sodium nitroprusside was gradually reduced and eventually stopped after 10 days, confirming the stability of the patient's clinical condition and normalisation of values.

An electrocardiogram taken at 7 and 20 days (Fig. 1b,c) and a chest X-ray (Fig. 2b) performed 15 days after hospital admission (when the patient had shown a clinical improvement) showed a near-complete regression of left ventricular hypertrophy and strain pattern, and normalisation of cardiac size (cardiothoracic ratio was 0.44). The MUGA scan was repeated approximately 20 days after hospital admission and showed an increase in left ventricular ejection fraction to approximately 65% (Fig. 3b). In addition, the echocardiogram at 20 days confirmed an improvement in and normalisation of left ventricular volumes, wall thickness, ejection fraction and filling pattern (Table 1).


   3. Discussion
Top
 1. Introduction
 2. Case report
 3. Discussion
References
 
Increased arterial pressure represents the most common cause of pressure overload and hypertrophy of the left ventricle, and plays a key role in the evolution of ventricular dysfunction and heart failure. The Framingham study reported that systemic hypertension was the underlying aetiology in approximately 75% of all subjects developing heart failure during follow-up [1,2].

Hypertensive crisis is characterised by a sudden increase in blood pressure—within minutes or hours (or days)—associated with or followed by signs of impairment of target organs (heart, kidney, brain). Patients with hypertensive crisis should be immediately treated with rapid-onset antihypertensive agents, such as sodium nitroprusside, nitroglycerin, diuretics, nifedipine, clonidine, dihydralazine and {alpha} and {alpha}–β blockers [3,6].

It has been reported that most patients with elevated blood pressure, particularly the elderly, experiencing acute pulmonary oedema have normal left-ventricular systolic function, suggesting that heart failure in these situations is due to diastolic dysfunction [1,7]. However, it has also been reported that uncontrolled systemic hypertension may be responsible for the development of left ventricular systolic dysfunction and heart failure, with consequent functional mitral regurgitation and subendocardial myocardial ischemia [8].

It has been reported that, in most cases of left ventricular systolic dysfunction clearly attributed to systemic hypertension, an improvement in clinical status and indices of cardiac function has been observed over a relatively long period of follow-up, which may be several months or even years [9–15].

It is of interest that in our patient, clinical status, left ventricular dilatation and systolic dysfunction dramatically improved in only a few days as a consequence of rapid blood-pressure normalisation, since other causes of left ventricular dysfunction had been accurately excluded. In fact, left ventricular ejection fraction and wall thickness normalised in approximately 3 weeks, together with an improvement in Doppler parameters of diastolic dysfunction (reduction of early filling peak velocity and prolongation of deceleration time of early filling), reflecting a reduction in left ventricular filling pressure.

Thus, we conclude that hypertensive crisis in our patient may have caused acute and severe left-ventricular systolic dysfunction (acute remodelling), creating a clinical picture of congestive heart failure and acute pulmonary oedema, reflecting an afterload mismatch of the left ventricle with exhaustion of the preload reserve [8]. The rapid reduction in elevated blood pressure by aggressive pharmacological treatment was essential to induce a regression of myocardial dysfunction in a very short time (reverse remodelling), which was associated with an improvement in clinical status. In this patient, assessment of left ventricular function, performed after clinical stabilisation, would have failed to identify the short-term systolic dysfunction and would have attributed the clinical condition to isolated diastolic dysfunction of the left ventricle. Accordingly, we conclude that the occurrence of left ventricular systolic dysfunction and hypertrophy, which is rapidly reversible with aggressive pharmacological therapy, should be taken into account when evaluating cardiac function in patients with acute pulmonary oedema due to uncontrolled hypertension in order to clarify the true pathogenic mechanism of the clinical condition.


   References
Top
 1. Introduction
 2. Case report
 3. Discussion
 References
 

  1. Verdecchia P., Schillaci G., Borgioni C. Prognostic significance of serial changes in left ventricular mass in essential hypertension. Circulation (1998) 97:48–54.[Abstract/Free Full Text]
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  4. Gandhi S.K., Powers J.C., Nomeir A.M., et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med (2001) 344:17–22.[Abstract/Free Full Text]
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  7. Little W.C. Hypertensive pulmonary oedema is due to diastolic dysfunction. Eur Heart J (2001) 22:1961–1964.[Free Full Text]
  8. Ross J. On variations in the cardiac hypertrophic response to pressure overload. Circulation (1997) 95:1349–1351.[Free Full Text]
  9. Dall'Aglio V., Nicolosi G.L., Burelli C. Echocardiographic findings of left ventricular hypertrophy and normalisation of parameters of left ventricular function in patients with previous evidence of dilated and poorly contracting left ventricle and coexisting systemic hypertension. Clin Cardiol (1989) 12:91–96.[CrossRef][Medline]
  10. Kramer K., Kirkman P., Kitzman D., Little W.C. Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization. Am Heart J (2000) 140:451–455.[CrossRef][Web of Science][Medline]
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