Myotonic dystrophy type 1 and high ventricular vulnerability at the electrophysiological evaluation: ICD yes or not?

A significant number of sudden death (SD) is observed in myotonic dystrophy (DM1) despite pacemaker implantation and some consider the ICD to be the preferential device in patients with conduction disease. According to the latest guidelines, prophylactic ICD implantation in patients with neuromuscular disorder should follow the same recommendations of non-ischemic dilated cardiomyopathy, being reasonable when pacing is needed. We here report a case of DM1 patient who underwent ICD implantation even in the absence of conduction disturbances on ECG and ventricular dysfunction/fibrosis at cardiac magnetic resonance. The occurrence of syncope, non-sustained ventricular tachycardias at 24-Holter ECG monitoring and a family history of SD resulted associated with ventricular fibrillation inducibility at electrophysiological study, favouring ICD implantation. On our advice, DM1 patient with this association of SD risk factors should be targeted for ICD implantation.

[The choked heart]. / Das abgewürgte Herz.

A couple of days after increasing the dosage of betaadrenergic- and adding calcium channel blockers due to an increased heart rate in atrial fibrillation, a 77 year old female was found in cardiogenic shock. After exclusion of further causes a therapy with catecholamines, calcium, high dose insulin and phosphodiesterase inhibitors was initiated. Despite this combined therapy the shock persisted. Only after administration of levosimendan, a calcium sensitizer, a normalization of the heart function could be observed. We discuss the danger of combining drugs with negative inotropic properties for rate control in atrial fibrillation and review the therapy with focus on the effects on cardiac cells of all recommended drugs in the treatment of intoxication with betareceptor- and calcium channel blockers.

[Clinical efficacy of antihypertensive therapy of pregnant women with arterial hypertension with long acting nifedipine and bisoprolol].

Study aim was assessment of clinical efficacy of mono therapy with nifedipine SR/GITS and combination of nifedipine SR/GITS and bisoprolol as well as investigation of functional state of sympathoadrenal system (SAS) in pregnant women with arterial hypertension. Examination and treatment with nifedipine SR/GITS 30 mg/day and bisoprolol 2,5 - 5 mg/day was carried out in 21 patients with stage II hypertensive disease (HD) during trimester II of pregnancy. Initially all women including 20 practically healthy pregnant women (control group) had elevation of functional activity of SAS what was determined by high values of b-adrenoception of membranes of erythrocytes. In patients with stage II HD this parameter significantly exceeded that of control group. Administration of antihypertensive drugs for 3 weeks promoted significant lowering of all parameters of 24 hour blood pressure monitoring down to optimal level, lessening of pathological types of 24 hour blood pressure profile and lowering of functional activity of SAS.

[Graves' disease and papillary thyroid cancer--coincidence or association?]. / Basedow-Struma mit papillärem Schilddrüsenkarzinom--Zufall oder Zusammenhang?

HISTORY AND ADMISSION FINDINGS: A 41-year-old woman presented with hyperhydrosis, tremor, restlessness, sleeplessness and diarrhea. She had a tachycardia and later she developed soreness of her conjunctives. A tender goitre could be palpated. INVESTIGATIONS: Laboratory results showed thryeotoxicosis and later elevated TRAK. Ultrasound revealed a thyroid nodule. Scintigraphic uptake was generally elevated. Graves disease was diagnosed. TREATMENT AND COURSE: After 12 months of thyreostatic medication recurrence occurred and a thyroidectomy was performed. Histologically a papillary cancer was found and postoperative radioiodinetherapy was added. CONCLUSION: Due to leading symptoms of thyreotoxicosis the thyroid nodule has preoperatively not been paid enough attention to. A pathophysiologic association of Graves disease and differentiated thyroid cancer is controversely discussed but seems possible considering present literature data. Scintigraphically "cold" nodules in graves disease, as in simple nodular goitre, have a higher probability of malignancy.

Practical recommendations for the use of ACE inhibitors, beta-blockers, aldosterone antagonists and angiotensin receptor blockers in heart failure: putting guidelines into practice.

Surveys of prescribing patterns in both hospitals and primary care have usually shown delays in translating the evidence from clinical trials of pharmacological agents into clinical practice, thereby denying patients with heart failure (HF) the benefits of drug treatments proven to improve well-being and prolong life. This may be due to unfamiliarity with the evidence-base for these therapies, the clinical guidelines recommending the use of these treatments or both, as well as concerns regarding adverse events. ACE inhibitors have long been the cornerstone of therapy for systolic HF irrespective of aetiology. Recent trials have now shown that treatment with beta-blockers, aldosterone antagonists and angiotensin receptor blockers also leads to substantial improvements in outcome. In order to accelerate the safe uptake of these treatments and to ensure that all eligible patients receive the most appropriate medications, a clear and concise set of clinical recommendations has been prepared by a group of clinicians with practical expertise in the management of HF. The objective of these recommendations is to provide practical guidance for non-specialists, in order to increase the use of evidenced based therapy for HF. These practical recommendations are meant to serve as a supplement to, rather than replacement of, existing HF guidelines.

Bisoprolol alone and in combination with amlodipine or nifedipine in the treatment of chronic stable angina.

Beta-blockers and calcium antagonists are both effective monotherapy for stable angina. When symptoms persist, these two agents are commonly co-prescribed in the hope that this combination has added benefit compared with monotherapy alone. We investigated the additional efficacy of the calcium antagonists amlodipine and nifedipine when added to bisoprolol in patients with stable angina. Patients were randomised in a multicentre, single-blind study, with crossover of three treatments consisting of bisoprolol 10 mg once daily, bisoprolol plus nifedipine 20 mg twice daily, and bisoprolol plus amlodipine 5 mg once daily. Exercise tests were performed at the end of each four-week study period and the exercise time to onset of angina was assessed. A total of 198 patients from 17 centres were recruited of whom 147 were evaluable for efficacy. There were no statistically significant differences in exercise duration to onset of angina between any of the groups. The combination of bisoprolol plus nifedipine was least well tolerated. In summary, this study suggests there is little benefit in adding a calcium antagonist to bisoprolol in treating patients with stable angina.

Medical treatment to reduce total ischemic burden: total ischemic burden bisoprolol study (TIBBS), a multicenter trial comparing bisoprolol and nifedipine. The TIBBS Investigators.

OBJECTIVES: We compared the effects of bisoprolol on transient myocardial ischemia with those of nifedipine in patients with chronic stable angina. BACKGROUND: Both beta-adrenergic blocking agents and calcium antagonists reduce transient ischemic episodes, but comparisons of these agents have been made in only a few larger studies. METHODS: The Total Ischemic Burden Bisoprolol Study (TIBBS) was a randomized double-blind controlled study with two parallel groups; 330 patients from 30 centers in seven European countries with stable angina pectoris, a positive exercise test and more than two transient ischemic episodes during 48 h of Holter monitoring (central evaluation) were included. Of these patients 161 were randomized to receive bisoprolol and 169 to receive nifedipine slow release. There were two treatment phases of 4 weeks each, with 48-h Holter monitoring after each phase. During phase 1, patients received either 10 mg of bisoprolol daily or 2 x 20 mg of nifedipine slow release. During phase 2, they received either 20 mg of bisoprolol daily or 2 x 40 mg of nifedipine slow release. RESULTS: In phase 1 of the trial, 4 weeks of bisoprolol therapy (10 mg daily) reduced the mean [+/- SD] number of transient ischemic episodes from 8.1 +/- 0.6 to 3.2 +/- 0.4/48 h. Nifedipine (2 x 20 mg) reduced transient ischemic episodes from 8.3 +/- 0.5 to 5.9 +/- 0.4/48 h. Total duration of ischemia was reduced from 99.3 +/- 10.1 to 31.9 +/- 5.5 min/48 h with bisoprolol and from 101 +/- 9.1 to 72.6 +/- 8.1 min/48 h with nifedipine. Reductions were statistically significant for both drugs; the difference between bisoprolol and nifedipine was also significant (p < 0.0001). Bisoprolol reduced the heart rate at onset of episodes by 13.7 +/- 1.4 beats/min from a baseline value of 99.5 +/- 1.2 beats/min (p < 0.001). Heart rate was unchanged with nifedipine. Bisoprolol had significantly higher responder rates than nifedipine. Doubling of the dose in phase 2 of the trial had small additive effects. Only bisoprolol showed a marked circadian effect by reducing the morning peak of transient ischemic episodes (by 68% at peak time, 8:00 to 8:59 AM). CONCLUSIONS: Both bisoprolol and nifedipine reduced the number and duration of transient ischemic episodes in patients with chronic stable angina. Bisoprolol was significantly more effective than nifedipine in both doses tested and reduced the morning peak of ischemic activity.

Study of the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease by programmed stimulation.

The objective of this study was to assess the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease (CAD) by programmed stimulation. Sixteen inpatients subjected to an electrophysiological investigation because of dizziness or palpitations were given 10 mg of intravenous bisoprolol after basal measurement and were checked again 15 and 45 min after infusion. Eight patients with CAD (seven males and one female; mean age of 60+/-4 years) and eight patients without CAD (five males and three females; mean age of 59+/-4 years) were investigated after washout of prior antiarrhythmic drugs. For coronary patients, the CAD was documented by a history of myocardial infarction or by a confirmatory coronary arteriography. Main outcome measures were parameters of invasive electrophysiological exploration, with measurement of conduction intervals at rest and during pacing and of refractory periods by means of extrastimulus technique. No significant difference was noted at baseline between the two groups except for CSNRT. After infusion of 10 mg of bisoprolol, with the exception of CSNRT (increased in the group without CAD), no significant differences were noted on comparison between coronary and noncoronary patients. Bisoprolol significantly increased the sinus cycle length, SACT, and FRP of the atria. Regarding atrioventricular nodal conduction, bisoprolol significantly increased the AH 100, ERP, and FRP and significantly decreased the Wenckebach point. In the right ventricle, bisoprolol moderately, but significantly, decreased the corrected QT and induced a small, temporary, significant increase in ERP. Bisoprolol appears to be a very potent beta-blocker that is well tolerated at an intravenous dose of 10 mg. Its depressant effects concern mainly the atrial function and the nodal conduction, without significant differences between the two groups of patients. The decrease in QTc may be a favorable aspect regarding its electrophysiologic tolerance especially in the acute phase of myocardial infarction.

Interaction of bisoprolol and procainamide in human cardiac impulse generation and conduction.

Combined treatment of beta-adrenoceptor-blocking agents and class I antiarrhythmic drugs can potentially have profound and deleterious effects on cardiac impulse formation and conduction. We studied the effect of 5 mg of oral bisoprolol daily and 10 mg/kg of procainamide intravenously with programmed electrical stimulation of the heart in 10 patients with postinfarction ventricular tachyarrhythmias. Oral bisoprolol slowed sinus rhythm and atrioventricular nodal conduction; ventricular effective refractory periods were increased significantly after several days of oral bisoprolol treatment. Combined treatment of oral bisoprolol and intravenous procainamide did not produce clinically relevant changes in parameters of cardiac impulse formation and conduction. This study shows that combined use of bisoprolol and a class I antiarrhythmic drug appears to be safe in patients with ventricular tachyarrhythrhythmias late after myocardial infarction.