Introduction: More women die of cardiovascular diseases than from any other illness. Evaluation of coronary artery disease (CAD) among premenopausal women has been neglected, since it is been considered to be rare. The purpose of this study was to compare the risk factor profile for CAD in premenopausal and postmenopausal Indian women presenting with acute coronary syndrome. Materials and Methods: This retrospective study was carried out at the Department of Cardiology, in a tertiary care cardiac center in Trivandrum, Kerala, India. Clinical and risk factor data were collected by reviewing hospital records. Coronary angiograms were assessed by two independent cardiologists. Results: A total of 232 patients were included in the study, of which 66 were in the premenopausal group with mean age of (45.85 ± 4.25) years, and 166 in the postmenopausal group with mean age of (67.40 ± 6.40) years. The incidence of hypertension (31 [46.96%] vs. 133 [80.12%], P < 0.001) and diabetes mellitus (28 [42.42%] vs. 104 [62.65%], P < 0.005) was higher among the postmenopausal women. ST elevation myocardial infarction was significantly higher (5 [7.57%] vs. 31 [18.67%], P = 0.035) among postmenopausal women. Coronary angiography showed that the premenopausal women had higher incidence of angiographically normal coronaries (27 [40.90%] vs. 37 [22.29%], P = 0.004), whereas postmenopausal women had more atherosclerotic triple vessel disease (7 [10.60%] vs. 46 [27.71%], P = 0.005). Conclusions: The CAD in premenopausal women is mostly nonatherosclerotic and nonobstructive. The conventional risk factors do not play a significant role among this subset of population.

Syncope is a transient loss of consciousness (LOC) due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery. Here, the term "transient LOC" encompasses all disorders characterized by self-limited LOC irrespective of the mechanism. Central point in pathophysiology of the development of syncope is fall in systemic blood pressure (BP) with a decrease in global cerebral blood flow. The evaluation and treatment of syncope are very challenging because syncope is not the only cause of transient LOC. Moreover, symptoms of syncope are fleeting, patient is usually asymptomatic at the time of evaluation, and most of the events are often unwitnessed. The guiding principle of assessment is to differentiate syncope from other causes of transient LOC and the more benign causes of syncope from the potentially serious ones. Initial assessment of syncope consists of a detailed history and examination complemented by 12-lead electrocardiography and supine and standing BP. If the cause is suspected, then further investigations may be needed to confirm the particular disorder. A deliberate approach based on initial risk stratification is more likely to give a correct diagnosis. Despite the difficulties, a thorough evaluation of the cause of syncope is warranted in all patients, not just in those deemed to be at high mortality risk. The goal in every case should be to determine the cause with sufficient confidence to provide a reliable assessment of prognosis and treatment options.

Fragmented QRS is defined as the presence of R' wave or notching of R or S wave in the presence of narrow QRS. It indicates heterogeneous depolarization of the ventricular myocardium that can occur due to ischemia, fibrosis, or scar. It may also be a marker of coronary microvascular dysfunction. In the context of epicardial coronary artery disease, it is associated with multivessel disease and greater incidence of cardiac events. It has been shown to be an indicator of higher incidence of arrhythmias and sudden death in arrhythmic right ventricular dysplasia, Brugada syndrome, and acquired long QT syndrome. Its regression following cardiac resynchronization therapy suggests electrical reverse remodeling. It has also been shown to be a marker of myocardial involvement in congenital heart diseases and is helpful in diagnosing subclinical cardiac involvement in various systemic diseases.

Studies from our laboratory at the University of Minnesota as well as that of others have demonstrated that agonist-mediated receptor stimulation leads to the activation of phospholipase C and formation of second messengers, diacyl glycerol and inositol trisphosphate, and mobilization of cytosolic free calcium. Elevation in intracellular calcium activates phospholipase A2 and release of arachidonic acid. This fatty acid is further converted to active metabolites, prostaglandin endoperoxides, and thromboxanes (TXA ₂ ). TXA ₂ promote fibrinogen binding, irreversible aggregation, and the release of granule contents, including serotonin and ADP. Agents that promote irreversible aggregation, facilitate fibrinogen binding, and those drugs that dissociate this process do so by lowering the cytosolic calcium levels. Endogenous antagonists such as PGE ₁ , PGI ₂ , and NO exert their inhibitory effect on platelet function by the action of cyclic nucleotides, cyclic AMP and cyclic GMP. Epinephrine-induced modulation of alpha-adrenergic receptor restores the action of agonists in drug-induced refractory platelets. As far as the role of cyclic nucleotides is considered, the observations are consistent with the concept that cyclic nucleotides participation in the biologic regulation may be modulated by cytoplasmic cations, and that a change in intracellular cyclic nucleotides and appropriate cations serves to promote the participation of both regulatory effectors. Anti-platelet drugs such as aspirin, indomethacin, and PGE ₁ do not inhibit platelet interactions with the vessel wall. Based on this collective knowledge, novel antiplatelet drugs should be developed for the prevention of acute vascular events.