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Secondary hypertension affects a small but significant number of the hypertensive population and, unlike primary hypertension, is a potentially curable condition. The determinant for workup is dependent on the index of suspicion elicited during patient examination and treatment. Specific testing is available and must be balanced depending on the risk and cost of the workup and treatment with the benefits obtained if the secondary cause is eliminated. This article reviews common manifestations, workup, and the current treatments of the common causes of secondary hypertension.

Refractory angina pectoris is defined as Canadian Cardiovascular Society class III or IV angina, where there is marked limitation of ordinary physical activity or inability to perform ordinary physical activity without discomfort, with an objective evidence of myocardial ischemia and persistence of symptoms despite optimal medical therapy, life style modification treatments, and revascularization therapies. The patients with refractory angina pectoris may have diffuse coronary artery disease, multiple distal coronary stenoses, and or small coronary arteries. In addition, a substantial portion of these patients cannot achieve complete revascularization and continue to experience residual anginal symptoms that may impair quality of their life and increase morbidity. This represents an end-stage coronary artery disease characterized by a severe myocardial insufficiency usually with impaired left ventricular function. As the life expectancy is increasing, patients with angina pectoris refractory to conventional antianginal therapeutics are a challenging problem. We review the nonconventional therapies to treat the refractory angina pectoris, including pharmacotherapy, therapeutic angiogenesis, transcutaneus electrical nerve and spinal cord stimulation, enhanced external counterpulsation, surgical transmyocardial laser revascularization, percutaneous transmyocardial laser revascularization, percutaneous in situ coronary venous arterializations, and percutaneous in situ coronary artery bypass. These therapies are not supported by a large body of data and have only a complementary role; therefore, the aggressive traditional and proven treatment of angina pectoris should be continued along with these therapies, used on an individual basis.

Cardiac troponins are highly specific markers of myocardial injury. It has been suggested that, unlike other markers of myocardial injury, troponins could be released in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes. Reversibly injury related changes in myocyte membrane are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of the myocytes. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility. The myocardial injury induced by diphtheric toxins could be completely reversible with successful treatment. We report a case of diphtheric myocarditis in a 20-year-old female who presented with complaints of dysphagia, dysphonia, fatigue, generalized malaise and severe dyspnea. She developed severe left ventricular systolic dysfunction (ejection fraction 10%) with markedly elevated serum levels of cardiac troponin I (peak 48.5 ng/ml). Within a few days on treatment, the cardiac function became completely normal (left ventricular ejection fraction 60%) and the elevation in serum level of cardiac troponin I resolved. This case supports the notion that cardiac troponin I could be released in reversible myocardial injury and that in such case the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness.

Left atrial volume index (LAVI) as a predictor of mortality has not been well investigated in patients with cardiac resynchronization therapy (CRT). The purpose of this study is to evaluate the impact of LAVI in predicting mortality in CRT patients.We studied 100 consecutive patients who received CRT (male 73, age 69.9 ± 9.6 years). The follow-up duration of all echocardiographic measurements was 14.4 ± 10.5 months after CRT. LAVI was measured from apical views on two-dimensional echocardiography by bi-plane rule. A decrease of left ventricular end systolic volume ≥ 15% after CRT was defined as a positive response to CRT.The mean LAVI at baseline was 59.9 ± 22.7 ml/m(2). LAVI in patients who died (78.2 ± 27.5 ml/m(2)) was significantly greater than those who survived (55.9 ± 19.5 ml/m(2), p0.0001) during follow-up of 17 ± 10.6 months. The area under ROC curve (AUC) for LAVI predicting death was 0.77 (p=0.0001). The cutoff point for LAVI predicting death was LAVI59.4 ml/m(2). LAVI59.4 ml/m(2) was related to mortality by Cox proportional univariate regression [hazard ratio (HR)=5.15, 95% CI=1.48-17.93, p=0.01]. After adjustment for the variables with significant difference by univariate regression, LAVI59.4 ml/m(2) was continuously related to mortality by multivariate regression (HR=4.56, 95% CI, 1.30-15.97, p=0.02). LAVI59.4 ml/m(2) was associated with a near 5-fold increase in mortality during follow-up of 17 ± 10.6 months.Patients who have LAVI59.4 ml/m(2) continue to have increased mortality despite CRT.

Atrioventricular node blocking agents including beta-adrenergic blockers, non-dihydropyridine calcium channel blockers and digoxin are usually effective in controlling ventricular rate in atrial fibrillation and flutter. Intravenous beta-blockers and non-dihydropyridine calcium channel blockers are equally effective in rapidly controlling the ventricular rate. The addition of digoxin to the regimen causes a favorable outcome but digoxin as a single agent is generally less effective in slowing the ventricular rate in acute setting. Clonidine, magnesium, and amiodarone have also been used for acute ventricular rate control in atrial fibrillation. Limited data suggest that combination regimens provide better ventricular rate control than any agent alone. The agent of first choice is usually individualized depending upon the clinical situation. Beta-blockers are preferable in patients with myocardial ischemia, myocardial infarction and hyperthyroidism and in post-operative state, but should be avoided in patients with bronchial asthma and chronic obstructive pulmonary disease where non-dihydropyridine calcium channel blockers are preferred. Beta-blockers are preferred drugs used for acute ventricular rate control in atrial fibrillation during pregnancy. In atrial fibrillation with Wolff-Parkinson-White syndrome, beta-blockers, calcium channel blockers and digoxin should be avoided, as these drugs are selective atrioventricular node blockers without slowing conduction through the accessory pathway, which can lead to increased transmission of impulses preferentially through the accessory pathway and precipitate ventricular fibrillation. The drug of choice for atrial fibrillation in pre-excitation syndrome is procainamide but propafenone, flecainide and disopyramide have also been used. When clinical condition is unstable or patient is hemodynamically compromised, immediate electrical cardioversion is the treatment of choice, as the best measure to control ventricular rate is by conversion to sinus rhythm. Factors precipitating rapid ventricular rate should be treated as well.

To evaluate the gender influence in diagnostic and prognostic value of Holter-detected ST-segment deviation.Two-hundred seventy-seven consecutive patients (196 men) who underwent coronary angiography for evaluation of chest pain were studied with 24-h Holter monitoring within 72 h of coronary angiography, and were followed up for 65+/-21 months.Men had a higher prevalence of coronary artery disease (169 of 196, 86%) compared to that of women (54 of 81, 67%), p0.00025. Thirty-three (17%) men and 15 (19%) women had ST-segment deviation during 24-h recording. The sensitivity, specificity and positive predictive values of ST-segment deviation (elevation, depression, or both) for the detection of significant coronary artery disease were similar in men and women. The negative predictive values were significantly higher in women than men for ST-segment deviation (36% vs. 15%, p0.001), ST-segment elevation (35% vs. 14%, p0.001), and ST-segment depression (34% vs. 15%, p0.001). Similarly, the diagnostic accuracies were significantly higher in women than men for ST-segment deviation (44% vs. 29%, p0.025), ST-segment elevation (38% vs. 19%, p0.001), and ST-segment depression (40% vs. 24%, p0.025). There was no significant difference in composite end-point of events (mortality, nonfatal myocardial infarction, unstable angina, and coronary revascularization) in men versus women with ST-segment deviation (elevation, depression, or both).Holter-detected ST-segment deviation has a higher negative predictive value and diagnostic accuracy for detection of significant coronary artery disease in women than in men, although the prognostic values are not significantly different between men and women.