Treatment of myotonia with antiarrhythmic drugs.

The effects of disopyramide, phenytoin, mexiletine, and tocainide were compared in 30 patients with myotonic disorders. The severity of myotonia was assessed by clinical and electromyographic criteria at the end of each treatment phase lasting four weeks. Mexiletine (MXT) and tocainide (TCD) were found to be the most potent antimyotonic agents. The antimyotonic efficacy of MXT and TCD is explained by their fast-blocking effect on voltage-dependent sodium channels in the muscle membrane. The benefits of myotonia control with pharmacological agents must be weight against the risk of therapy in the individual patient. Because of the risks of hematologic problems, TCD is not recommended by us for the treatment of myotonia.

The correlation between CK MB curve type and the clinical course of recent myocardial infarction.

In 265 patients with acute myocardial infarction (MI) for whom the 72-hour CK MB curve was obtained, three types of a curve were found: with a single and early 16 h peak value (type A), with a single late 16 h peak value (type B), and with a double peak (type C). Type A of the CK MB curve was found in 32% of patients with acute MI, type B in 55% and type C in 13%. There were no significant differences of CK MB max between the type groups. Infarct size differed significantly between groups (A-29 +/- 19, B-35 +/- 22, C-53 +/- 30 g Eq CK MB). In-hospital mortality also differed significantly particularly between type C (31%) and type A groups (5%). Nitroglycerin or practolol given intravenously during the first 48 hours changed the CK MB curve mainly by decreasing CK MB max as compared to controls treated conventionally. There was no effect of treatment with either nitroglycerin or practolol on the clinical course in patients with type A CK MB curve. There is a good correlation between the CK MB curve type and the clinical course of MI. Nitroglycerin or practolol decreased the infarct size only in patients with either B or C type of CK MB curve, having no influence in patients with a mild form of acute MI (type A).

Significance of anterior precordial ST-segment depression in acute inferior myocardial infarction.

In 70 consecutive patients (pts) with acute transmural inferior infarction, 58 had significant precordial ST depression (group A) and the remaining 12 had no ECG changes in precordial leads (group B) on admission. At the time of hospital discharge, the persistence of anterior ST depression was observed in 13 pts (group A1), normalization in 45 (group A2). Infarct size was significantly greater (p less than 0.05) in group A than in group B (37.6 vs. 23.8 CK-MB gEq). The largest infarct (51.5 CK-MB gEq) and the most serious clinical course was observed in group A1. No significant differences were noticed in the frequency of reinfarction and episodes of acute coronary insufficiency during hospitalization and one-year follow-up between groups. Persistent precordial ST depression is a simple ECG marker of extensive infarction, left ventricular dysfunction and a worse clinical course.

The effect of infarct size on atrioventricular and intraventricular conduction disturbances in acute myocardial infarction.

The effect of infarct size estimated from serial CK-MB isoenzyme determinations on the incidence of atrioventricular and intraventricular conduction disturbances was examined in 250 patients suffering their first myocardial infarction. The size of the infarct was significantly greater (P less than 0.001) in 72 patients with conduction disturbances than in 178 without conduction defects (54 +/- 29 vs. 35 +/- 22 CK-MB gEq). The largest size was observed in 10 patients with bifascicular block (71 +/- 38 CK-MB gEq). Within the group of patients with intraventricular conduction disturbances, the size of the infarct was significantly greater (P less than 0.01) when localized inferiorly rather than anteriorly (91 +/- 10 vs. 58 +/- 27 CK-MB gEq). The size in those patients with complete atrioventricular block and anterior infarction was larger than in those with an inferior lesion (76 +/- 21 vs. 52 +/- 33 CK-MB gEq). The size in those patients with inferior infarction and complete block was significantly greater (P less than 0.05) than in patients with similarly positioned infarction without conduction disturbances (52 +/- 33 vs. 35 +/- 22 CK-MB gEq). There was no significant difference in the size of infarct when inferior infarction was complicated by first- and second-degree block in comparison to those without conduction defects (38 +/- 23 vs. 35 +/- 22 CK-MB gEq). A correlation was observed between the size of infarction and the incidence of conduction disturbances (P less than 0.001); the greater the size the higher the incidence of conduction disturbances.

Haemodynamic effects of nitroglycerin infusion in patients with postinfarction heart failure.

On the basis of their own 5-year experience, the authors discuss the indications for, and limitations of, intravenous infusion of nitroglycerin (NTG). In 42 patients with postinfarction heart failure, NTG produced a significant reduction of left ventricular filling pressure, regardless of its initial value. In patients with normal or only slightly elevated left ventricular filling pressure, NTG caused a decrease in cardiac index and mean arterial pressure as well as, in the earliest phase of infusion, an increase in peripheral resistance. Similar trends were observed also in patients with markedly elevated left ventricular filling pressure if mean arterial blood pressure fell by more than 20%. Taking into consideration that the range of the effective doses was very wide (15-150 micrograms/min), the authors believe that intravenous NTG infusion is indicated mainly in cases of manifest heart failure and should be administered under strict control of the dosage and with careful monitoring of the therapeutic effects.

Vasodilator drugs in patients with chronic ischaemic heart failure.

The effects of intravenous nitroglycerin (NTG), trimetaphan (TMP), and phentolamine (PTL) on pulmonary artery diastolic pressure (PADP), systemic arterial pressure (SAP), cardiac index (CI) and systemic vascular resistance (SVR) in patients (12 in each treated group) with chronic ischaemic heart failure are analyzed. Each group was divided into two subgroups according to the initial PADP taking into account the mean value in the whole group. A significant decrease in PADP (by 40%; p less than 0.001) was observed in the NTG-treated group, with no significant changes in CI and SVR except for patients with moderately elevated initial PADP, in whom SVR increased slightly in the early period of treatment, and CI decreased (by 25%; p less than 0.05). TMP and PTL reduced SVR (by 25 and 30% respectively; p less than 0.01) and increased CI irrespective of the initial PADP. TMP significantly decreased PADP in patients in whom its level was initially high. The results suggest that NTG is mainly a venodilating agent which should be used in patients with high PADP and normal or slightly decreased CI. PTL acts mainly by reducing SVR and increasing CI. TMP influences both PADP and SVR and is a drug of choice in patients with high or elevated PADP and low cardiac output.

Beneficial effects of intravenous nitroglycerin on haemodynamics and enzymatically estimated infarct size.

The effects of intravenous nitroglycerin (TNG) were evaluated in 39 patients with a first acute myocardial infarction, subdivided according to Killip into those with left ventricular failure (N = 24) and those without (N = 15). A group of 38 randomly selected patients treated in a conventional, but unstandardized manner, served as a control (C). TNG caused a statistically significant reduction in pulmonary artery diastolic pressure, regardless of its initial value, by about 30%. Neither cardiac index nor total peripheral resistance was significantly changed. Infarct size, measured in gEq of isoenzyme MB creatine kinase (CK-MB), was smaller by about 40% in both subgroups of patients treated with TNG, when compared with the controls. A significant difference was found in peak CK-MB blood levels only in the group of patients with left ventricular failure (Killip classes II and III) treated with TNG. The best results were obtained when TNG was given not later than 4 h after the onset of the symptoms of infarction.