In a patient with multiple CVRF with concomitant heart and renal failure (presumably of multiple etiology: renal hypoperfusion, arteriosclerosis...), we must be very careful when using diuretics and ACEI/ARA-II, since we can worsen renal function and/or increase potassium levels (among diuretics, spironolactone and eplerenone are "potassium-sparing"). Therefore, in this case we will use bisoprolol.

A 75-year-old man, hypertensive and dyslipidemic with a history of heart failure due to left ventricular systolic dysfunction (EF < 30%). He comes to our office for worsening of his usual dyspnea in recent weeks. His systolic blood pressure is 160/95 mmHg with a heart rate of 65 bpm. In the physical examination no crackles were heard and his jugular venous pressure was normal. He provides a creatinine determination that is 3.7 mg/dL with ions within normal. Which of the following drugs is the most appropriate to improve the prognosis of his heart failure?

A Case of Refractory Heart Failure in Becker Muscular Dystrophy Improved With Corticosteroid Therapy.

The patient was a 26 year-old man who was referred to our hospital in June 2011 because of severe heart failure. At age 24 years, he was found to have Becker muscular dystrophy. He received enalapril for cardiac dysfunction; however, he had worsening heart failure and was thus referred to our hospital. Echocardiography showed enlargement of the left ventricle, with a diastolic dimension of 77 mm and ejection fraction of 19%. His condition improved temporarily after an infusion of dobutamine and milrinone. He was then administered amiodarone for ventricular tachycardia; however, he subsequently developed hemoptysis. Amiodarone was discontinued and corticosteroid pulse therapy was administered followed by oral prednisolone (PSL). His creatinine phosphokinase (CPK) level and cardiomegaly improved after the corticosteroid therapy. The PSL dose was reduced gradually, bisoprolol was introduced, and the catecholamine infusion was tapered. A cardiac resynchronization device was implanted; however, the patient's condition gradually worsened, which necessitated dobutamine infusion for heart failure. We readministered 30 mg PSL, which decreased the CPK level and improved the cardiomegaly. The dobutamine infusion was discontinued, and the patient was discharged. He was given 7.5 mg PSL as an outpatient, and he returned to normal life without exacerbation of the heart failure. There are similar reports showing that corticosteroids are effective for skeletal muscle improvement in Duchenne muscular dystrophy; however, their effectiveness for heart failure has been rarely reported. We experienced a case of Becker muscular dystrophy in which corticosteroid therapy was effective for refractory heart failure.

[An elderly man with known heart failure admitted with cardiogenic shock].

A 75-year-old man with post-MI heart failure and an ejection fraction of 15 % was treated with an ACE-inhibitor, spironolactone and a beta-blocker. He had reduced his intake of food and water due to an intercurrent illness the days before admission. He was admitted to our coronary care unit due to bradycardia and hypotension. On arrival his blood pressure was 60/40 mm Hg, and he was in a cardiogenic shock. The electrocardiogram showed broad QRS-complexes and large T waves. Serum-potassium was 9.1 mmol/L and he had acute renal failure with oliguria, probably caused by reduced cardiac output due to hypovolemia combined with taking an ACE inhibitor and spironolactone. Haemodialysis was started and during dialysis QRS complexes became more narrow and heart rate and blood pressure normalized. The patient was discharged 10 days later with normal potassium and creatinine levels. Patients treated with ACE-inhibitors and spironolactone should be monitored closely. During intercurrent illness dehydration may occur and this can lead to renal failure and hyperkalemia which can be life-threatening. The condition should be recognized and addressed promptly, and if indicated haemodialysis should be performed.

ECG of the month. Irregular rhythm in a 25-year-old man with three prior cardiac operations. Coarse atrial fibrillation with a rapid ventricular response, left anterior fascicular block, left ventricular hypertrophy with repolarization abnormality.

The patient underwent closure of an atrial septal defect at age 3, had a leaking "mitral" valve repaired at age 9, and at age 13 had a "mitral" valve replacement. He began taking warfarin sodium at that time and remained symptom-free until 10 days before his initial visit here when he presented to another hospital with dyspnea and palpitations. Treatment there consisted of lisinopril 10 mg qd, carvedilol 6.25 mg bid, aldactone 25 mg qd, furosemide 40 mg qd, digoxin 0.25 mg qd, and a continuation of warfarin sodium 7.5 mg qd. An echocardiogram showed a left ventricular ejection fraction of 20%. After diuresis, he was referred to our cardiology clinic. On his initial visit here, his heart rate was an irregular 120 beats/min, his blood pressure was 106/77 mmHg, and closing and opening snaps of a normally functioning mechanical mitral valvular prosthesis were heard. He was obese (height, 5' 9"; weight, 272 lbs). An electrocardiogram was recorded (Figure 1).

Heart failure with preserved ejection fraction

Although the term diastolic heart failure is often used when there are signs and symptoms of heart failure with normal left ventricular systolic function, this is not always appropriate. Diastolic function is determined by the relative end diastolic volume in relation to end diastolic pressure, and is therefore independent of left ventricular systolic function. A leftward shift of the end-diastolic pressure-volume relationship (i.e. decreased left ventricular distensibility) can occur both in those with normal and those with decreased left ventricular systolic function. Likewise, heart failure may occur in those with dilated left ventricular and normal systolic function. This is often seen in valvular heart disease and high-output heart failure. Neither of these situations constitutes a diastolic heart failure. Stiffening of the left ventricle contributes heart failure with preserved ejection fraction, a condition that can be prevented with exercise.

Cases from the Osler Medical Service at Johns Hopkins University.

PRESENTING FEATURES: A 70-year-old African American man was admitted with a history of fever, chills, and malaise of several days' duration. His past medical history was notable for end-stage renal disease requiring hemodialysis, coronary artery disease, and aortic stenosis requiring a bioprosthetic aortic valve replacement. On the day of admission, the patient was noted to have a shaking chill while undergoing dialysis through his catheter and was admitted to the hospital. He complained of pain at the catheter insertion site, shortness of breath, and dyspnea on exertion, but denied chest pain. On physical examination, the patient had a temperature of 100.4 degrees F, with a heart rate of 64 beats per minute, blood pressure of 127/72 mm Hg, and an oxygen saturation of 97% on room air. He was a mildly obese man in no apparent distress. He had shotty cervical lymphadenopathy and a right subclavian dialysis catheter in place, with erythema and pus at the entry site. His jugular venous pressure was 10 cm H(2)O. Lung examination showed bibasilar rales. Heart sounds were normal, with no rub or gallop. He had a 2/6 systolic ejection murmur best heart at the left sternal border as well as a 3/6 holosystolic murmur at the apex that radiated to his left axilla. Examination of the abdomen and extremities was unremarkable. The patient's neurological examination was unremarkable, and he was alert and oriented to person, place, and time. Laboratory studies showed an elevated white blood cell count of 16,700 cells/microL. His blood urea nitrogen level was 43 mg/dL and his serum creatinine level was 4.9 mg/dL. Multiple blood cultures grew methicillin-resistant Staphylococcus aureus. An admission, chest radiograph showed no infiltrate. An admission electrocardiogram showed normal sinus rhythm with first degree atrioventricular block, left anterior fascicular block, and left ventricular hypertrophy. shows rhythm strips from lead II electrocardiograms 5 months before admission (top), on admission (middle) and 5 days after admission (bottom). What is the diagnosis?

Left ventricular diastolic heart failure with normal left ventricular systolic function in older persons.

Underlying causes and precipitating causes of congestive heart failure (CHF) should be treated when possible. Older persons with CHF and normal left ventricular (LV) ejection fraction should have maintenance of sinus rhythm, treatment of hypertension and myocardial ischemia, slowing of the ventricular rate below 90 beats/minute, and reduction of salt overload. First-line drug treatment in the management of these persons is the use of loop diuretics combined with beta blockers as tolerated. Angiotensin-converting enzyme (ACE) inhibitors should be administered if CHF persists despite diuretics and beta blockers. If persons are unable to tolerate ACE inhibitors because of cough, rash, or altered taste sensation, angiotensin II type 1 receptor antagonists should be given. If CHF persists despite diuretics, beta blockers, and ACE inhibitors or the person is unable to tolerate beta blockers, ACE inhibitors, and angiotensin II type 1 receptor antagonists, isosorbide dinitrate plus hydralazine should be administered. Calcium channel blockers should be used if CHF persists despite administration of diuretics and the person is unable to tolerate beta blockers, ACE inhibitors, angiotensin II type 1 receptor antagonists, and isosorbide dinitrate plus hydralazine. Digoxin, beta blockers, verapamil, and diltiazem may be used to slow a rapid ventricular rate in persons with supraventricular tachyarrhythmias. Digoxin should not be used in persons with CHF in sinus rhythm with normal LV ejection fraction.

[Successful use of angiotensin II receptor antagonist (losartan) in a patient with scleroderma renal crisis].

A 67-year-old man with a one-and-a half-year history of Raynaud's phenomenon was admitted to our hospital for progressive dyspnea occurring over the previous two weeks. Physical examination revealed a blood pressure of 200/124 mmHg, and slightly tight and smooth skin of the fingers, hands and forearms. Laboratory evaluation included serum creatinine of 5.42 mg/dl, plasma renin activity > 20 ng/ml/hr, and antinuclear antibody with a titer of 1 : 1,280. Renal biopsy was performed and the histopathological findings showed that some glomeruli exhibited ischemic retraction with wrinkling of the basement membranes, and that one arteriole exhibited significant intimal hyperplasia with luminal stenosis. These findings were compatible with scleroderma renal crisis (SRC). On the 5th day, serum creatinine had risen to 9.16 mg/dl, and he required temporary hemodialysis therapy. After the administration of captopril was started, his blood pressure fell to 160/86 mmHg and serum creatinine was reduced to 5.12 mg/dl. On the 9th day, he exhibited skin eruptions, and captopril was discontinued accordingly and temocapril started. Because of continued eruptions, temocapril was replaced by losartan. His blood pressure was controlled easily and his serum creatinine level reduced steadily. One year after the start of losartan, serum creatinine was 2.25 mg/dl and blood pressure was 130/82 mmHg. SRC is a life-threatening manifestation of systemic sclerosis. In the late 1970s, angiotensin converting enzyme (ACE) inhibitor was introduced and has dramatically improved the outcome in SRC patients. As ACE inhibitors act mainly on hyperreninemic renal vasoconstrictive hypertension in SRC, we would expect losartan, a selective antagonist of angiotensin receptor subtype 1, to be interchangeable with ACE inhibitors in SRC. In 1997, Caskey and colleagues reported the failure of losartan to control hypertension in a patient of SRC, and the reason has remained unclear. We report here, a case of SRC whose blood pressure was controlled successfully and his renal failure reversed by the administration of losartan.

Pharmacologic therapy for patients with chronic heart failure and reduced systolic function: review of trials and practical considerations.

Heart failure (HF) is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricles to fill with or eject blood. The approach to pharmacologic treatment has become a combined preventive and symptomatic management strategy. Ideally, treatment should be initiated in patients at risk, preventing disease progression. In patients who have progressed to symptomatic left ventricular dysfunction, certain therapies have been demonstrated to improve survival, decrease hospitalizations, and reduce symptoms. The mainstay therapies are angiotensin-converting enzyme (ACE) inhibitors and beta-blockers (bisoprolol, carvedilol, and metoprolol XL/CR), with diuretics to control fluid balance. In patients who cannot tolerate ACE inhibitors because of angioedema or severe cough, valsartan can be substituted. Valsartan should not be added in patients already taking an ACE inhibitor and a beta-blocker. Spironolactone is recommended in patients who have New York Heart Association (NYHA) class III to IV symptoms despite maximal therapies with ACE inhibitors, beta-blockers, diuretics, and digoxin. Low-dose digoxin, yielding a serum concentration <1 ng/mL can be added to improve symptoms and, possibly, mortality. The combination of hydralazine and isosorbide dinitrate might be useful in patients (especially in African Americans) who cannot tolerate ACE inhibitors or valsartan because of hypotension or renal dysfunction. Calcium antagonists, with the exception of amlodipine, oral or intravenous inotropes, and vasodilators, should be avoided in HF with reduced systolic function. Amiodarone should be used only if patients have a history of sudden death, or a history of ventricular fibrillation or sustained ventricular tachycardia, and should be used in conjunction with an implantable defibrillator [corrected]. Finally, anticoagulation is recommended only in patients who have concomitant atrial fibrillation or a previous history of cerebral or systemic emboli.

ECG Case of the Month: Heart Failure in a Man from Chile.

A 49-year-old man visiting New Orleans from Chile comes to the hospital complaining of exertional dyspnea for 2 months with the more recent onset of ankle edema. He is a slender man with a blood pressure of 91/60 mmHg, crackles at both lung bases, and markedly distended neck veins. His cardiac rhythm is irregular. A soft murmur of mitral regurgitation and a soft S-3 are heard at the left ventricular apex. All four pedal pulses are easily palpable. Epigastric tenderness is noted on palpation; although the patient has a history of peptic ulcer disease, the tenderness is probably due to an enlarged left lobe of his liver, the result of hepatic congestion from his heart failure. A chest radiograph shows generalized cardiomegaly with an especially large left ventricle. Pulmonary congestion and small bilateral pleural effusions also are noted. The Figure shows the electrocardiogram recorded on admission.

Update of treatment of heart failure with reduction of left ventricular ejection fraction.

Underlying and precipitating causes of heart failure (HF) with reduced left ventricular ejection fraction (HFrEF) should be identified and treated when possible. Hypertension should be treated with diuretics, angiotensin-converting enzyme (ACE) inhibitors, and β-blockers. Diuretics are the first-line drugs in the treatment of patients with HFrEF and volume overload. Angiotensin-converting enzyme inhibitors and β-blockers (carvedilol, sustained-release metoprolol succinate, or bisoprolol) should be used in treatment of HFrEF. Use an angiotensin II receptor blocker (ARB) (candesartan or valsartan) if intolerant to ACE inhibitors because of cough or angioneurotic edema. Sacubitril/valsartan may be used instead of an ACE inhibitor or ARB in patients with chronic symptomatic HFrEF class II or III to further reduce morbidity and mortality. Add an aldosterone antagonist (spironolactone or eplerenone) in selected patients with class II-IV HF who can be carefully monitored for renal function and potassium concentration. (Serum creatinine should be ≤ 2.5 mg/dl in men and ≤ 2.0 mg/dl in women. Serum potassium should be < 5.0 mEq/l). Add isosorbide dinitrate plus hydralazine in patients self-described as African Americans with class II-IV HF being treated with diuretics, ACE inhibitors, and β-blockers. Ivabradine can be used in selected patients with HFrEF.

Pulmonary artery ablation to treat pulmonary arterial hypertension: a case report.

Idiopathic pulmonary arterial hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance that results in right heart failure and premature death. Although therapies exist to improve hemodynamic instability and symptoms, there is no cure for pulmonary arterial hypertension and it remains a life-threatening condition. A recent study performed in China reported, for the first time, the effect of pulmonary arterial denervation on functional capacity and hemodynamics in patients with refractory idiopathic pulmonary arterial hypertension. We report a case of a 60-year-old white Brazilian man, with controlled hypertension and stage 2 obesity who complained of progressive fatigue with moderate to light exertion of approximately 1 year's duration. During this period, he underwent myocardial perfusion scintigraphy without evidence of obstructive ischemic disease. He had no clinical evidence of systolic heart failure. He had undergone biological mitral valve replacement 3 years previously for mitral valve stenosis and ablation of atrioventricular nodal reentry tachycardia 18 months previously. At the time of valve replacement, he had no reported evidence of pulmonary arterial hypertension. His echocardiogram showed normal function of a mitral prosthesis, normal global left ventricular systolic function (left ventricular ejection fraction 62 % measured using the Teichholz method), stage I diastolic dysfunction, and a mean systolic pulmonary arterial blood pressure of 50 mmHg. In the 6-minute walk test, the patient walked 104 meters. Catheterization of his right heart chambers and pulmonary arteries confirmed the diagnosis of pulmonary hypertension. Electroanatomic reconstruction of the right ventricular outflow tract and pulmonary artery was performed under direct fluoroscopic visualization, and a merger was made with a formatted image of cardiac computed tomography angiography. Then we performed irrigated cardiac catheter ablation of the pulmonary trunk. At the patient's 3-month follow-up, he showed improvement in functional class for fatigue on major exertion, increased distance walked in the 6-minute walk test, and reductions in pressure of both the right cavities and the pulmonary artery. Currently, with 6 months of clinical follow-up, the patient has maintained his functional classification and is pedaling his bicycle.

Treatment of heart failure with normal left ventricular ejection fraction.

Underlying causes and precipitating causes of heart failure (HF) should be treated when possible. Persons with HF and normal left ventricular ejection fraction (LVEF) should have maintenance of sinus rhythm, treatment of hypertension, myocardial ischemia, dyslipidemia, and anemia, slowing of the ventricular rate below 90 bpm, and reduction of salt overload. First-line drug treatment in the management of these persons is the use of loop diuretics combined with beta blockers and angiotensin-converting enzyme (ACE) inhibitors. If persons are unable to tolerate ACE inhibitors because of cough, angioneurotic edema, rash, or altered taste sensation, angiotensin II type I receptor antagonists (ARBs) should be given. If HF persists despite diuretics, beta blockers, and ACE inhibitors or ARBs, isosorbide dinitrate plus hydralazine should be administered. Beta blockers, verapamil, diltiazem, and digoxin may be used to slow a rapid ventricular rate in persons with supraventricular tachyarrhythmias. Digoxin should not be used in persons with HF in sinus rhythm with normal LVEF. Exercise training should be encouraged in persons with mild to moderate HF to improve functional status and to decrease symptoms.

TIMI

TIMI Risk Score for STEMI Age 65-74 years? Yes (+2) – or – Age ≥75 years? Yes (+3) Diabetes, Hypertension or Angina? Yes (+1) Systolic BP < 100 mmHg? Yes (+3) Heart rate > 100? Yes (+2) Killip Class II-IV (JVD or any pulmonary exam findings of CHF)? Yes (+2) Weight < 67kg (147.7 lbs)? Yes (+1) Anterior ST Elevation or LBBB? Yes (+1) Time to treatment > 4 hours? Yes (+1) What Does This Score Mean? TIMI Risk Score for HF in Diabetes Prior heart failure? Yes (+2) History of atrial fibrillation? Yes (+1) Coronary artery disease? Yes (+1) eGFR < 60 ml/min/1.73*m2? Yes (+1) Urine albumin-to-creatinine ratio >300 mg/g? Yes (+2) – or – Urine albumin-to-creatinine ratio 30-300 mg/g? Yes (+1) What Does This Score Mean?

[A 91-year-old man with a stroke, hypertension, and renal failure].

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.

Recent developments in the management of heart failure.

The typical presentation of heart failure in primary care is insidious, with progressive breathlessness on exertion, ankle swelling, orthopnoea or paroxysmal nocturnal dyspnoea. Not all patients will have all these symptoms, and in many patients there may be other causes. If a GP suspects heart failure, then the key blood test is B-type natriuretic peptide (BNP). If the BNP is normal then heart failure is unlikely and other diagnoses should be considered. If it is raised, or if there is a past history of myocardial infarction, the patient requires further assessment, which must include echocardiography and a specialist assessment. The underlying cardiac abnormality should be identified. An ECG is often very useful and if it is completely normal it makes heart failure less likely. Both the NICE and the ESC guidance emphasise the importance of lifestyle management (regular appropriate exercise, avoiding excessive salt and alcohol consumption). ACE inhibitors (or angiotensin receptor blockers) and beta-blockers licensed for heart failure (carvedilol, bisoprolol, nebivolol) remain the mainstay of treatment in addition to as small a dose of diuretic as possible to control any fluid retention. Aldosterone antagonism is recommended by the 2012 ESC guidance for all patients who remain symptomatic despite an ACE inhibitor and beta-blocker. If the rhythm is sinus but the heart rate is 75 beats per minute, therapy needs to be optimised, perhaps by increasing the beta-blocker dose, if possible, or by the addition of ivabradine.

[A comparison of the clinical efficacy of enalapril maleate analogs in patients with heart failure and ischemic heart disease].

The authors examined 68 patients aged from 42 to 68 years with ischemic heart disease without a history of myocardial infarction and with angina pectoris of exertion functional class 2-3 and circulatory insufficiency class 2 (according to NYHA criteria). The criteria serving as the reason for relating patients to the follow-up group were left-ventricular end-diastolic volume > 160 ml, ejection fraction < 30%, cardiothoracic index > 0.55, threshold power of endured loads within a range of 71.5 +/- 2.30 watt. After stabilization of the clinical status by means of basic therapy (nitrates, blockers of slow calcium channels, diuretics, antiaggregants), all patients were divided into two follow-up groups. The first group consisted of 36 patients who received renitec (10 mg/24 h), patients of group 2 were given enap in the same dose. The course of treatment lasted 12 weeks. The effectiveness of treatment was controlled by echocardiography according to the standard methods in M- and B-regimens. Analysis of the obtained data showed that within 12-day follow-up renitec demonstrated higher effectiveness and lesser incidence of side-effects than did enap given in the same dose.

Management of heart failure

Beta blockers Until recently (within the last 20 years), β-blockers were contraindicated in CHF, owing to their negative inotropic effect and ability to produce bradycardia – effects which worsen heart failure. However, current guidelines recommend β-blocker therapy for patients with systolic heart failure due to left ventricular systolic dysfunction after stabilization with diuretic and ACEI therapy, irrespective of symptomatic severity or blood pressure. As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, nebivolol and extended-release metoprolol. The antagonism of β1 inotropic and chronotropic effects decreases the amount of work the heart must perform. It is also thought that catecholamines and other sympathomimetics have an effect on cardiac remodeling, and blocking their activity can slow the deterioration of cardiac function.

[Heart function and clinical observations of patients with severe congestive heart failure treated with milrinone].

To evaluate the clinical effects of milrinone in patients with severe heart failure, heart function and clinical observations were performed on 25 patients with severe congestive heart failure treated with domestic intravenous milrinone for 15 days. Results showed that the total response rate to milrinone was 96% while 60% of them had significant improvement. Heart function and diameter of left atrial, left ventricle, and right ventricle were measured by pulsed Doppler and M-mode echocardiographg before and after the treatment. The systolic function of the left ventricle (such as SV, CO, EF, FS, IVST, PLVWT) was significantly improved. The diastolic function of the left ventricle (such as E peak, A peak, IRT) was also improved. Diameter of left atrial, left ventricle, and right ventricle was significantly reduced. The heart rate and blood pressure remained unchanged. No obvious side-effect was found in our observation. The domestic intravenous milrinone is a drug of choice for the management of patients with severe congestive heart failure.

Implantation of a Jarvik 2000 left ventricular assist device as a bridge to eligibility for refractory heart failure with renal dysfunction.

A 55-year-old man, who previously underwent surgical ventricular restoration and mitral valve surgery, was referred to our department for management of refractory heart and multiple organ failure. At the time of admission to our hospital, he could not be registered as a candidate for heart transplantation because of severe renal failure with a serum creatinine level of 4.6 mg/dl. We considered that he was a marginal candidate for heart transplantation; thus, it was essential to understand the etiology of renal failure and estimate whether it was reversible. Cardiac catheterization revealed poor hemodynamic function with a systemic pressure of 107/60 mmHg, cardiac index of 2.5 l/min/m(2), and pulmonary artery pressure of 63/27 mmHg, despite intense medical treatment. Contrary to biochemical examination findings of blood, renal biopsy findings showed no significant glomerular abnormality. Furthermore, the severity of tubular atrophy and interstitial fibrosis in the cortex was mild. These pathological findings suggested that the renal dysfunction in this case was possibly attributable to a hemodynamic factor. His symptoms gradually deteriorated despite an increasing dose of inotropic support; thus, we planned implantation of a Jarvik 2000 axial-flow pump (Jarvik Heart Inc., New York, NY, USA) as a bridge to eligibility, and informed consent was obtained. Because of a tight adhesion on the anterior wall, we placed the device on the lateral wall of the left ventricle, making sure not to direct the pump at the septum. Postoperatively, the implantable left ventricular assist device provided relief from heart failure symptoms as well as recovery of renal function, with serum the creatinine level at 1.2 mg/dl, which allowed the patient to become an appropriate candidate for heart transplantation. At an 18-month follow-up examination, his status was uneventful, and he is now at home awaiting heart transplantation.

[Trends in pharmacological treatment of congestive heart failure].

Congestive heart failure (CHF) is growing epidemiologic and clinical problem, and is the only common cardiovascular condition that is increasing in incidence, prevalence and mortality. During last years numerous clinical trial have been conduced evaluating the effect of various treatment procedures on clinical endpoints in patients with CHF. The major risk factor for CHF are hipertension and atherosclerotic vascular diseases, and now it is clear that aggressive treatment of hypertension and hyperlipidemia can be effective in preventing CHF. Treatment strategies for CHF are aimed at preventing and delaying progression of the disease and improving survival. In the treatment of CHF diuretics are at present the first drugs line for patients with fluid retention and are necessary to relieve symptoms but cannot halt progression or improve the prognosis of CHF. Angiotensin-converting enzyme inhibitors (ACE inhibitors) therapy has been shown to decrease mortality and progression of CHF and should be used early in patients with left ventricular dysfunction whether they have symptomatic or asymptomatic CHF. Digoxin therapy is associated with decrease in the risk of worsening CHF irrespective of rhythm, systolic function, severity of CHF or therapy with ACE inhibitors. In patients with symptomatic CHF due to systolic dysfunction the addition of diuretics and digoxin appears to reducing worsening CHF without improving survival. Other than digoxin oral inotropic agents (amrinone, pimobendan, vesnarinone, ibopamine) increase mortality in patients with CHF and have not improved symptom status and other clinical endpoints during long-term therapy. Hydralazine and isosorbide dinitrate administrated in combination are less effective alternative to ACE inhibitors. Beta-blockers and particular carvedilol may prolong survival and decrease worsening CHF when used in combination with digoxine, diuretics and ACE inhibitors. Beta-blockers therapy improve hemodynamics, LVEF and functional status patients with CHF and the ideal candidate for this therapy is stable patients with NYHA II-III CHF due to nonischemic cause. Calcium antagonists do not appear to be useful in patients with CHF, although amlodipine and mibefradil appears to be safe for treatment of angina or hypertension in this group. On the basis of current data, antiarrhythmic agents should not be given to patients with CHF free from arrhythmia but those with sustained ventricular tachycardia or ventricular fibrillation amiodaron appears to be safe.

[A 46-year-old man with cardiac failure and statues epileptics].

We report a 46-year-old man with bacterial endocarditis and cardiac failure, who developed status epileptics. The patient was apparently well until July of 1991 when there was a gradual onset of fever and general fatigue. He was hospitalized to the cardiology service of our hospital where diagnosis of bacterial endocarditis and aortic insufficiency was made. On October 9, 1991, he suddenly developed cardiogenic shock, and emergency replacement of the aortic valve was made; at the operation, the main trunk of the left coronary artery showed embolic occlusion, and the myocardial movement was markedly diminished; serum creatine kinase was 3.150 IU/l. His cardiac failure did not resolve, and renal failure developed in December 1991, for which peritoneal dialysis was necessary. On February 2, 1992, he suddenly developed a clonic seizure which started from his face with a transient post-ictal left hemiparesis; a cranial CT scan was unremarkable. He was treated with phenytoin and glycerol, however, he developed status epileptics on February 3; he developed cardiac arrest after the injection of phenytoin 750 mg. He was resuscitated, however, his status did not resolve. Neurological consultation was asked on February 4. On physical examination, his blood pressure was 80/40 mmHg heart rate 77/min and regular, and body temperature 39.1 degrees C. The palpebral conjunctiva were slightly anemic, however, the bulbar conjunctiva were not icteric. No cervical adenopathy was noted. Glade II systolic murmur was heard in the apex; the lungs were clear. The abdomen was flat and soft without organomegaly. No edema was present in the legs. On neurologic examination, he was comatose without response to painful stimuli. He repeatedly had convulsion lasting for 30 seconds every 2 to 3 minutes; his convulsions started with the conjugate deviation of the eyes to the left followed by turning of the head toward left, and then clonic convulsions started in this left upper limb extending to other extremities. The optic fundi were unable to visualize because of corneal clouding; light reflex was sluggish on the right side; no oculocephalic response was elicited; corneal reflex was also lost bilaterally. Extremities were hypotonic, and no automatic movement was seen. The triceps brachii reflex was diminished, but all the other deep reflexes were lost; no plantar response was elicited. Meningeal sign was absent. He was treated with intravenous diazepam; the interval of convulsions prolonged, however, blood pressure dropped to 40 to 40 mmHg. On February 4, intravenous thiopental anesthesia was instituted, and assisted respiration was started.(ABSTRACT TRUNCATED AT 400 WORDS)

[Effects of enalapril on left ventricular hypertrophy in patients with mild or moderate essential hypertension].

To evaluate the effects of enalapril maleate on the regression of left ventricular hypertrophy (LVH) associated to hypertension. Fifteen male, age between 45 and 65 years (mean age = 56 y) with diagnosis of mild-to-moderate essential hypertension (greater than diastolic blood pressure [DBP] less than between 90 and 114 mmHg) and LHV at the echocardiogram. The administration of enalapril maleate was initiated with a 20 mg daily dosage and titrated up to a maximum of 40 mg daily, whenever DBP was maintained above 90 mmHg and no adverse experience occurred. Fourteen patients completed the clinical trial and all of them achieved satisfactory blood pressure (BP) control. The dosage of enalapril was 20 mg/day for 11 patients and 40 mg/day for the other three. The mean systolic blood pressure in supine position decreased from an initial value of 151.4 +/- 9.5 to 126.4 +/- 9.4 mmHg at the end of treatment and the mean diastolic blood pressure from 100.0 +/- 5.0 to 80.4 +/- 1.5 mmHg (p less than 0.001). There was a reduction of mean diastolic septal wall thickness from 11.5 +/- 0.05 to 10.1 +/- 0.05 mm and left ventricular posterior wall thickness from 11.2 +/- 0.7 to 9.8 +/- 0.6 mm (p less than 0.05). The diastolic dimension and left ventricular volume did not show significant changes. The mean of calculated left ventricular mass showed a decrease from 263.6 +/- 32.9 to 231.3 +/- 34.7 g at the end of treatment (p less than 0.05). Mean ejection fraction and fractional fiber shortening showed light, but non significant increase. The tolerability to the drug was satisfactory. Two patients complained of transient palpitations and two other, irritative cough, that determined the treatment discontinuation in one case. Enalapril maleate 20 to 40 mg daily, besides the satisfactory control of BP in patients with mild-to-moderate essential hypertension, promoted regression of left ventricular hypertrophy, without impairment of left ventricular function.

Atherosclerotic Renovascular Disease.

The patient, a 78-year-old Asian male, was brought to the hospital because of acute shortness of breath that had progressively worsened over the course of the day. He complained of a nonproductive cough and claudication after walking 1 block. His past medical history was significant for mild renal insufficiency (serum creatinine 1.5--2.0 mg/dl), the etiology of which was never explored. Although there was a recent history of mild to moderate hypertension, at presentation his blood pressure was noted to be 240/118 mm Hg in both arms. His physical exam at the time of admission was remarkable for grade II hypertensive retinopathy, an S4 gallop, periumbilical systolic bruits, audible femoral arterial bruits and absent distal lower extremity pulses. Initial complete blood count, serum electrolytes and cardiac enzymes (including lactate dehydrogenase) were normal. His blood urea nitrogen and serum creatinine concentrations were 51 and 3.6 mg/dl, respectively, and his urinalysis showed 1+ protein (both by dipstick and sulfasalicylic acid) with a "benign" sediment (0--1 WBC/HPE, 1--2 RBCs/HPF) with occasional granular casts. His electrocardiogram, apart from demonstrating left ventricular hypertrophy with secondary ST-T wave abnormalities, showed no acute changes; his chest X-ray demonstrated cardiomegaly and pulmonary vascular congestion. He was intubated and subsequently treated with increasing parenteral doses of furosemide (40--240 mg) and a nitroglycerine drip (up to 15 mcg/min). Over the course of the first 48 h, his blood pressure was gradually lowered to 170/100 mm Hg. His urine output increased from 20 ml/h to 125/ml/h, and his respiratory status improved, allowing him to be extubated. In spite of adequate control of his blood pressure in the ensuing days (150--170/80--90 mm Hg), his renal function continued to deteriorate. Renal sonography (without Doppler) demonstrated a right kidney of 9.6 cm and a left kidney of 9.3 cm in length without evidence of hydronephrosis. Both kidneys were noted to be echogenic. Assays for antinuclear antibodies and antineutrophilic cytoplasmic antibodies were negative, and the patient's serum complement levels were normal. For several days after his admission, his serum creatinine gradually rose to 10.7 mg/dl, and hemodialysis was initiated for uremic encephalopathy. Because of the high index of suspicion for renal artery stenosis as the case of both his hypertension and renal failure, a renal angiogram was performed. It revealed a 90% occlusion of the right renal artery with ostial involvement and a 70% occlusion of the left renal artery; both kidneys had poor distal renal vasculature and there was marked atherosclerotic disease of the aorta. After being hemodialyzed for 3 treatments, his renal function began to improve spontaneously. His serum creatinine returned to 3.4 mg/dl, and a subsequent 24-hour urine demonstrated a creatinine clearance of 20 ml/min and an excretion of 1.2 g of protein. Following his discharge from the hospital, his renal function remained unchanged for 3 years, and his blood pressure was easily controlled on monotherapy with a long-acting calcium channel blocker. He recently died from pneumonia.

[Value of heart rate recordings in selecting the initial treatment of hypertension].

60 patients with mild arterial hypertension are studied, divided into three groups according to their heart rate (HR): 20 with heart rate below 70 b.p.m.; 20 with heart rate between 70 and 80 b.p.m., and 20 with heart rate above 80 b.p.m. In every group, 10 patients were treated with atenolol and the other 10 patients with chlorthalidone. The cases of bad tolerance or bad response to any of these drugs were included in the other subgroup, so that a total number of 71 responses to drugs were studied. It has been found that the hypertension in patients having HR above 80 b.p.m. has a better response to atenolol. On the other hand, in patients having HR below 70 b.p.m. the response is better to chlorthalidone. In those patients with HR between 71 and 79 a similar response to both drugs is observed, nevertheless the decrease of the diastolic pressure is significantly bigger with atenolol. We arrive at the conclusion that when the HR is above 70 b.p.m. and especially above 80 b.p.m., better results are obtained using atenolol than chlorthalidone.

A Case of Dapsone-induced Mild Methemoglobinemia with Dyspnea and Cyanosis.

Dear Editor, Dapsone is a dual-function drug with antimicrobial and antiprotozoal effects and anti-inflammatory features (1). In dermatology, it is a first choice for conditions such as leprosy, IgA pemphigus, dermatitis herpetiformis, and linear IgA bullous dermatosis, or an adjunctive treatment for, e.g. bullous pemphigoid (BP) and pemphigus vulgaris (1). However, dapsone is associated with some adverse effects, including methemoglobinemia (1). Methemoglobin (MetHb) concentrations of less than 15% usually cause no symptoms in patients with normal hemoglobin concentrations (2). Herein, we report the case of a patient with BP who developed dyspnea because of dapsone-induced methemoglobinemia that was as mild as 4.7%. A 93-year-old man was diagnosed with BP based on skin manifestations (Figure 1, a and b), histopathological findings (Figure 1, c and d), and anti-BP180 NC16A antibody titer determined by chemiluminescence enzyme immunoassay (279 U/mL) 3 years earlier. His comorbidities included diabetes mellitus, chronic heart failure, right pleural effusion, and brain infarction. The patient had been successfully treated with oral prednisolone, so the steroid was tapered to 4 mg/day. The blisters recurred, however, and new ones kept developing even though the prednisolone was increased to 25 mg/day. Dapsone (75 mg/day) was begun as adjunctive treatment, and new blister formation ceased. At one week from dapsone initiation, the patient developed dyspnea, and his oxygen saturation as measured by pulse oximetry decreased to 88% on room air. At presentation, his blood pressure was 118/78 mmHg, the heart rate was 95 beats/minute, and axillary temperature was 36.3 °C. Neurological examination and consciousness findings remained unchanged compared with findings before dyspnea onset. Chest examination showed normal breath and heart sounds, but lip and peripheral cyanosis was present. Blood tests revealed a white blood cell count of 12,920/μl; red blood cells, 370×104/μl; hemoglobin, 11.7 g/dl; and CMV antigenemia (or C7-HRP), negative. Chest CT and echocardiography indicated no remarkable change compared with imaging from one year earlier. Arterial blood gas analysis showed a pH of 7.454, PaO2 63.1 mmHg, PaCO2 35.4 mmHg, HCO3- 24.3 mmol/L, SaO2 92.4%, and MetHb of 4.7%. These findings indicated a saturation gap (difference between SpO2 and SaO2) induced by MetHb. Upon cessation of dapsone, MetHb levels and SpO2 returned to normal and the dyspnea resolved, implicating dapsone in the methemoglobinemia (Figure 1, e). Differential diagnoses were pulmonary disease, heart disease, neuromuscular disease, sepsis, and drug intoxication. These possibilities were ruled out by the physical examination, drug history, vital signs, blood tests, and chest CT and echocardiography. In normal individuals, MetHb levels are less than 1% (2). Healthy patients with normal hemoglobin concentrations develop cyanosis at MetHb level of 15-20%, dyspnea at 20-50%, and coma at 50-70%, and die at more than 70% (2). However, patients with hematologic disease, acidosis, or cardiopulmonary diseases, for example, present with symptoms even with MetHb levels less than 15% (2,3). We inferred that our patient presented with dyspnea even under mild methemoglobinemia because he had anemia, chronic heart failure, and right pleural effusion. The occurrence of dapsone-induced methemoglobinemia with obvious symptoms is rare (1,4). Clinicians should be aware that methemoglobinemia symptoms are influenced not only by MetHb concentrations but also by comorbidities.

[The effect of hypotensive drugs on left ventricular mass and diastolic function].

Chronic left ventricular hypertrophy (LVH) is associated with depressed contractile performance, abnormal compliance of the chamber, and ultimately, the development of a left ventricular failure. Thus the presence of LVH carries a particularly ominous prognosis in patients with essential hypertension. Finally, regression of LVH appears to be a worthwhile goal of an antihypertensive therapy along with blood pressure control. Of particular importance, is whether the functional derangements associated with hypertrophy will also be reversed. The present study was undertaken to determine whether antihypertensive therapy reduced ventricular mass, and whether these changes were accompanied by improved diastolic function. 47 patients with mild-to-moderate essential hypertension were divided into two groups. Group I--included 21 patients whose blood pressure responded to nifedipine monotherapy. Group II--included 26 patients whose normalization of blood pressure required combined therapy with nifedipine and metoprolol. 40 healthy volunteers comprised a control group. To assess the effects of antihypertensive therapy on the heart, left ventricular mas (LVM), systolic and diastolic function, by M-mode, 2-D and pulsed wave Doppler echocardiography had been evaluated. Measurements were performed before therapy and every 3rd month during first year, and every 40th month during the second year of observation. RESULTS. At baseline all hypertensive patients had significantly increased LVM compared to the controls. Indexes of systolic function in studied patients were normal, while indexes of LV diastolic filling were significantly abnormal compared to the controls. In the group treated with nifedipine, starting from the 9th month of observation, small but significant decrease in posterior wall thickness was noted but LVM did not change during the whole time of the observation. Similarly, there was no significant change in indexes of left ventricular diastolic filling. Contrary to patients treated with nifedipine, in group of patients treated with combination of nifedipine and metoprolol, significant reduction of LVM and improvement of LV diastolic filling was observed. Of particular interest was the fact, that improvement in diastolic, performance appeared earlier, and preceded regression of LVM. Most striking was the improvement in Ev/Av ratio which increased by 16% after 6 months and by 35% after 24 months of the therapy. CONCLUSION. 1. Combined therapy with nifedipine and metoprolol contrary to monotherapy with nifedipine alone, results in the regression of left ventricular mass and the improvement of left ventricular diastolic function. 2. Improvement of left ventricular diastolic function appears earlier, preceding the regression of left ventricular hypertrophy.

Miliary tuberculosis in an immunocompetent male with a fatal outcome.

A man aged 33 years, born in Nepal, but resident in the UK for 7 years presented to the emergency department with a 4-day history of general malaise, fever (temperature 38.6°C) and a non-productive cough. His medical history was unremarkable and no high-risk behaviour was identified. Clinical examination confirmed decreased air entry bilaterally with bibasal crackles. He was tachycardic, with a heart rate of 120 bpm. Further investigation with a 12-lead ECG confirmed supraventricular tachycardia (SVT) which was terminated with vagal manoeuvres. His chest radiograph demonstrated left basal consolidation. His white cell count was 11×10<sup9</sup/L and his C reactive protein was 43.2 mg/L. His blood cultures revealed no growth. He was diagnosed with community-acquired pneumonia and started treatment with amoxicillin and clarithromycin. 3 days post admission, he was intubated for 24 hours in the Department of Intensive Care Medicine. Further episodes of SVT were observed and an ECHO showed a severely dilated and impaired left ventricle. Further chest radiographs illustrated diffuse consolidation with evidence of pulmonary oedema. HIV serology was negative. He developed transaminitis and thrombocytopenia. An ultrasound scan of his liver showed no obvious liver pathology. He remained tachypnoeic and due to worsening pulmonary oedema and extensive consolidation, he was readmitted to the intensive care unit. A CT abdomen with contrast showed an unusual pattern of lymphadenopathy with disproportionately enlarged coeliac axis nodes (5×7×5 cm) and minor para-aortic adenopathy, suspicious for lymphoma. On inserting his central venous catheter in his right internal jugular vein, pus was inadvertently aspirated from his right neck. Acid alcohol fast bacilli (AAFFB) were isolated from the pus and was subsequently identified as Mycobacterium tuberculosis He started treatment with antitubercular medication rifater: a combination of rifampicin 720 mg od, isoniazid 300 mg po od and pyrazinamide 1750 mg. In addition, he received ethambutol 1000 mg po od and pyridoxine 5 mg. He developed worsening metabolic acidosis, pH 7.19, loss of respiratory compensation and pancytopenia. Right heart strain was evident on his Focused Intensive Care Echo. He developed an increased oxygen requirement and respiratory distress on the ventilator. An erect chest radiograph showed bilateral pneumothoraces and bronchopleural fistulae. A chest drain was inserted. Following discussion with the Cardiothoracic Surgeons, pleurodesis was not deemed possible. He developed inotropic-dependent shock with worsening lung compliance. As a result of his deteriorating ventilation, acidosis and hyperkalaemia, he started treatment with continuous veno-venous haemofiltration. With a diagnosis of miliary tuberculosis and SVT causing cardiogenic pulmonary oedema, this man sadly died with his family at his bedside 10 weeks following initial hospital presentation.

[Comparative study of 2 diuretic-containing combination preparations in patients with edematous heart failure].

The efficacy and tolerability of two combinations, namely 50 mg spironolactone + 20 mg furosemide (SF) or 50 mg spironolactone + 5 mg butizide (SB), were compared in a randomised intraindividual trial in 22 patients with congestive heart failure. The parameters used were: weight, ankle- and calf-circumference, blood pressure, resting pulse, resting ECG, spirometry and blood chemistry. The physicians' judgement of the success of treatment was also recorded. Clinical symptoms improved clearly in both groups and in most cases there was significant improvement of the various parameters. The trend towards improvement was more apparent with SF. The physicians considered SF to be more effective in 12 cases compared to one case with SB. In all other cases both treatments were considered equally effective. The blood chemistry data showed relevant differences: serum-potassium levels were less scattered with SF and showed a - desirable - shift into the upper normal range. The number of patients with elevated serum-creatinin-levels increased during SB-treatment whereas the opposite was noted with SF. This could be due to furosemide's positive effects on renal functions.

A Case Report of Renal Sympathetic Denervation for the Treatment of Polymorphic Ventricular Premature Complexes: Expanding Horizons.

Premature ventricular complexes are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Recently, Armaganijan et al reported the relevance of sympathetic activation in patients with ventricular arrhythmias and suggested a potential role for catheter-based renal sympathetic denervation in reducing the arrhythmic burden. In this report, we describe a 32-year-old hypertensive male patient presenting with a high incidence of polymorphic premature ventricular complexes on a 24  hour Holter monitor. Beginning 1 year prior, the patient experienced episodes of presyncope, syncope, and tachycardia palpitations. The patient was taking losartan 100  mg/day, which kept his blood pressure (BP) under control, and sotalol 160  mg twice daily. Bisoprolol 10  mg/day was used previously but was not successful for controlling the episodes. The 24  hour Holter performed after the onset of sotalol 160  mg twice daily showed a heart rate ranging between 48 (minimum)-78 (average)-119 (maximum) bpm; 14,286 polymorphic premature ventricular complexes; 3 episodes of nonsustained ventricular tachycardia, the largest composed of 4 beats at a rate of 197 bpm; and 14 isolated atrial ectopic beats. Cardiac magnetic resonance imaging with gadolinium perfusion performed at rest and under pharmacological stress with dipyridamole showed increased left atrial internal volume, preserved systolic global biventricular function, and an absence of infarcted or ischemic areas. The patient underwent bilateral renal sympathetic denervation. The only drug used postprocedure was losartan 25  mg/day. Three months after the patient underwent renal sympathetic denervation, the mean BP value dropped to 132/86  mmHg, the mean systolic/diastolic 24  hour ambulatory BP measurement was reduced to 128/83  mmHg, and the 24  hour Holter monitor showed a heart rate ranging between 51 (minimum)-67 (average)-108 (maximum) bpm, 854 polymorphic premature ventricular complexes, and no episodes of nonsustained ventricular tachycardia.

Electrocardiographic strain pattern and prediction of new-onset congestive heart failure in hypertensive patients: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study.

The ECG strain pattern of ST depression and T-wave inversion is strongly associated with left ventricular hypertrophy (LVH) independently of coronary heart disease and with an increased risk of cardiovascular morbidity and mortality in hypertensive patients. However, whether ECG strain is an independent predictor of new-onset congestive heart failure (CHF) in the setting of aggressive antihypertensive therapy in unclear. The relationship of ECG strain at study baseline to the development of CHF was examined in 8696 patients with no history of CHF who were enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study. All patients had ECG LVH by Cornell product and/or Sokolow-Lyon voltage criteria on a screening ECG, were treated in a blinded manner with atenolol- or losartan-based regimens, and were followed up for a mean of 4.7+/-1.1 years. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite the QRS axis in lead V5 or V6. ECG strain was present in 923 patients (10.6%), and new-onset CHF occurred in 265 patients (3.0%), 26 of whom had a CHF-related death. Compared with patients who did not develop CHF, hypertensive patients who developed CHF were older; were more likely to be black, current smokers, and diabetic; were more like to have a history of myocardial infarction, ischemic heart disease, stroke, or peripheral vascular disease; and had greater baseline severity of LVH by Cornell product and Sokolow-Lyon voltage, higher baseline body mass indexes, higher serum glucose levels and albuminuria, similar baseline systolic and diastolic pressures, and reductions in diastolic pressure with treatment but greater reductions in systolic pressure. In univariate Cox analyses, ECG strain was a significant predictor of new-onset CHF (hazard ratio [HR], 3.27; 95% CI, 2.49 to 4.29) and CHF mortality (HR, 4.74; 95% CI, 2.11 to 10.64). In Cox multivariable analyses adjusting for baseline differences between patients with and without new-onset CHF, in-treatment differences in systolic and diastolic pressures, Sokolow-Lyon voltage, and Cornell product, and the impact of treatment with losartan versus atenolol on outcomes, ECG strain remained a significant predictor of incident CHF (HR, 1.80; 95% CI, 1.30 to 2.48) and CHF-related death (HR, 2.78; 95% CI, 1.02 to 7.63). ECG strain identifies hypertensive patients at increased risk of developing CHF and dying as a result of CHF, even in the setting of aggressive blood pressure lowering.

A Rare Case of Isolated Left Ventricular Non-compaction in an Elderly Patient.

A 61-year-old male, with a history of emphysema, obstructive sleep apnea, and hypertension, presented to the emergency room with worsening shortness of breath over a three-month period. The patient also complained of orthopnea, paroxysmal nocturnal dyspnea, and progressively worsening lower limb swelling. On examination, the patient had jugular venous distension, bilateral lower extremity edema, and bibasilar crackles. The laboratory evaluation showed an elevated B-natriuretic peptide level and a normal troponin level. A transthoracic echocardiogram (TTE) showed a reduced left ventricular ejection fraction (LVEF) of 20%-25% with prominent hyper-trabeculations noted in the left ventricle, most prominent in the lateral and apical walls. These findings were concerning for left ventricular non-compaction (LVNC). The patient underwent left heart catheterization, which did not show obstructive coronary disease as a cause of his cardiomyopathy. The patient was managed with guideline-directed therapy for heart failure and was started on warfarin due to the increased risk of thromboembolism associated with LVNC. During his admission, he exhibited multiple episodes of nonsustained ventricular tachycardia and was subsequently evaluated by electrophysiology (EP). He was discharged home with a wearable cardioverter defibrillator with instructions to follow up with EP in three months for an evaluation of implantable cardioverter-defibrillator (ICD) placement for primary prevention.

[Problem in the management of arterial hypertension resistent to drug treatment. Study of 28 cases].

The antihypertensive effect of the following therapeutic regimens: diuretic alone (DA), diuretic plus sympathetic inhibitor (DSI), diuretic plus betablocker (DB) and diuretic plus, betablocker plus vasodilator (DBV) was studied for 34.1 +/- 5.4 months in 28 patients with resistant essential hypertension (REH). Depending of treatment tolerability and the optimal antihypertensive action of drugs 21, 24, 26 and 10 cases were treated continuously or alternately with DA (9.9), DSI (15.0), DB (4.8), and DBV (14.6), respectively (in paragraph average duration of treatment in months). On admission the 89.3% and 42.8% of population had electrocardiographic signs of left ventricular hypertrophy or past-history of cardio-vascular complications, respectively. Arithmethic average and standard deviation of individual changes of systolic and diastolic blood pressure obtained during DA, DSI, DB and DBV treatment were -32.4 +/- 31.8, -19.3 +/- 27.2, -18.9 +/- 15.9 and -18.2 +/- 21.3 for systolic and -35.8 +/- 20.2, -12.3 +/- 17.2, -15.1 +/- 16.9 and -15 +/- 13.1 (mm. de Hg.) for diastolic blood pressure respectively. Average blood pressure before treatment was 222.4 +/- 30.3/128.0 +/- 20.8 (mm of Hg) and under the most effective treatment was 175.5 +/- 21.8/106.5 +/- 12.1 with a p less than or equal to 0.001 for either sistolic and diastolic pressure. There were not significant regressive electrocardiographic changes during the therapeutic period, neither significant changes in urea and creatinine blood values. 46.4% and 25% of cases exhibited collateral drug symptoms and cardio-vascular no fatal complications, respectively. Three of the last group patients died outside of the Hospital (2 sudden deaths and 1 renal insufficiency death). RH still constitutes a challenge to medical therapy. Nevertheless individualized therapy may modify the natural history of this hypertensive variety.