Acute termination and chronic prevention of supraventricular tachycardias; a comparative study between two calcium channel blockers: diltiazem and verapamil

Acute termination of paroxysmal supraventricular tachycardias [SVT] can be usually achieved by interrupting reciprocation at the level of AV node using calcium channel blockers. The study compared the safety and effectiveness of intravenous preparation [IV] of verapamil versus diltiazem in the termination of paroxysmal SVT and the oral therapy for the prevention of recurrence during a follow up period of three months. A baseline blood pressure [BP], Hr and 12 lead electrocardiogram [FCC] followed by IV drug in group [A] verapamil in a dose of 0.075 mg/kg and in group [B] diltiazem in a dose of 0.25 mg/kg over two minutes was used. In both groups, if SVT did not terminate within 15 minutes, a second dose is followed. BP and ECG monitoring were recorded immediately, five, ten and fifteen minutes after injection. If there is failure of termination of SVT after the second dose and/or the Pt develops complication [hypotension or hypersensitivity reaction], termination by DC is tried. For each patient converted to sinus rhythm, an oral dose of either drug [verapamil 240 mg/d and diltiazem 180 mg/d] is prescribed and patients were followed every two, four, eight and twelve weeks. The results revealed that termination of STV could be achieved in 90% of all patients with paroxysmal STV. No significant difference in conversion rate of both drugs [86.7% in verapamil versus 93.3% in diltiazem] was found. In 19 patients with STV due to AVNRT, verapamil could terminate STV in 98% versus 100% by diltiazem [p=NS]. Also, both drugs had the same conversion rate [80%] in ten patients with STV due to AVRT=AP. Both IV drugs were well tolerated and did not cause significant drop in BP. During mean follow up period of two months, 66.6% on oral verapamil versus 53.8% on oral diltiazem had no recurrence [p=NS]

Comparison of left ventricular function in insulin and non-insulin dependent diabetes mellitus

This study aimed to evaluate the effect of insulin- [IDDM] and non- insulin-dependent [NIDDM] DM on the left ventricular [LV] function. Forty diabetic patients [twenty NIDDM and twenty IDDM] and twenty control cases were included in the study. These patients underwent clinical examination, resting electrocardiogram, treadmill stress test and 2-D and Doppler echocardiography. The patients were divided into two groups [both groups had a negative treadmill exercise test]: Group I included ten normal subjects [mean age 31 +/- 7.8 years] compared with IDDM patients [mean age 32.4 +/- 8.1 years] and Group II included ten normal subjects [mean age 44.5 +/- 4.4 years] compared with NIDDM patients [mean age 43 +/- 4.5 years]. It was concluded that diabetic patients without clinical evidence of heart disease had both systolic and diastolic dysfunction. IDDM showed more frequent echocardiographic systolic and diastolic abnormalities than NIDDM independent of coronary artery disease

Effect of beta blocker therapy on the clinical status and hemodynamic parameters in patients with chronic heart failure

Recent trials reported that beta blockers [BB] might have some beneficial effects on congestive heart failure [CHF] that might be related to reduction in excessive adrenergic stimulation to the failing heart. However, most of the trials were not placebo- controlled. In order to evaluate such beneficial effects, 18 patients with CHF and fractional shortening [FS] <20% were randomly assigned to receive either placebo [P] or metoprolol [M], the B1-selective BB [11 M and 7 P]. M was titrated from 25 mg/day to a target dose of 150 mg/day. The mean daily dose of M was 118 mg [ranging from 100 mg to 150 mg]. All patients were treated with digoxin, diuretics and ACE inhibitors. They were followed up for three months. Patients were assessed before and after treatment regarding the clinical condition, New York Heart Association functional class [NYHA FC] and echocardiographic parameters [left ventricular end-systolic dimension [ESD] in cm, end-diastolic dimension [EDD] in cm, ejection fraction [EF%] and end systolic stress [ESS0 in g/cm2 at rest [R] and during hand grip exercise [HG EX]]. Clinical assessment was done by scoring of the clinical condition giving one point for each of the following: Breathlessness on exertion, pulmonary rates, S3 gallop, increased jugular venous pressure <6 cm above the angle of Lewis, heart rate >100 beats/min and the presence of pulmonary congestion on chest X- ray

Acute phase reactant CRP and ESR versus cardiac enzymes in evaluation of the extent of active coronary artery disease [unstable angina and acute myocardial infarction]

Acute phase reactant C-reactive protein [CRP] and the erythrocyte sedimentation rate [ESR] are expected to rise during the course of active coronary artery disease [CAD] [unstable angina [UA] and acute myocardial infarction [M.I.] as an inflammatory process has been proposed to be involved in the pathogenesis of both conditions. Our aim of this study was to evaluate the kinetics of rise of CRP and ESR and their correlation with the pattern of changes of cardiac enzymes [creation phospokinase [CPK], lactic dehydrognase [LDH] and serum glumatic oxalacetic transferase [SGOT] in active CAD. 50 patients [pts] with active CAD were studied [17 pts with UA [gp. I]; including 12 males and 5 females with a mean age of 53.4 +/- 7y and 33 pts with acute M.I. [gp. II]; including 24 males and 4 females with a mean age of 54.2 +/- 11y. The mean CRP and ESR were elevated in gpi [2.12 +/- 1.12 mg/dl and 58.7 +/- 33 mm/h respectively with the serial cardiac enzymes [CPK, LDH and SGOT] were within normal limits. Gp II revealed marked elevations of the cardiac enzymes [CPK ranged from 202-1800 IU/L with a mean of 774 +/- 448 while the mean peak LDH was 1093 +/- 400 IU/L [315-2080 IU/L] mean SGOT was 157 +/- 98 U/L [20-400 U/L]. Serum CRP was significantly elevated ranged 6-24 mg/dl with a mean of 18 +/- 5.6 mg/dl and the mean ESR was 83 +/- 33 mm/h ranged from 25-140 mm/h]. For CRP the mean time to peak was 3.15 +/- 0.69 and mean time to disappear was 8.53 +/- 0.91 d after the onset of chest pain. Strong correlation was found between mean CRP and Mean CPK [r=0.5]. Also, Significant difference was found between peak CPK in pts with anterior and inferior M.I. [p> 0.05]. We conclude that: The concentration of CRP rapidly in response to tissue injury [acute M.I.] with a peak level at a mean time of 60 hours after chest pain, falls to normal after 7 days in uncomplicated cases. A significant correlation was found between CPK, CRP and ESR as indices of severity in pts suffering from acute M.I. A positive CRP test is a valuable aid in establishing the presence of irreversible injury and the more the area of myocardial necrosis, the more prolonged the production and the persistence of the postulated mediato

Silent myocardial ischemia in-patients on chronic hemodialysis

Various factors may contribute to myocardial ischemia in patients on chronic hemodialysis. Ten asymptomatic non-diabetic patients, with normal resting electrocardiogram and echocardiogram on chronic regular hemodialysis, were studied for silent ischemia using 24-hour Holter ECG monitor. In conclusion, the main risk factors for coronary artery disease did not differentiate patients at increased risk for silent myocardial ischemia. Silent ischemia occurs more in the post dialysis period and thus can be explained by hypovolemia, hypotension and tachycardia rather than by hypoxia