Background: Periodontal disease is characterized by inflammation and destruction of supporting tissues of the affected teeth. Pro-inflammatory cytokines originating at the site of local pathology activate hepatocytes to produce acute-phase proteins including C-reactive protein (CRP). Numerous cross-sectional studies have suggested that chronic periodontitis is a risk factor for cardiovascular disease (CVD) linked by inflammatory factors including CRP. Materials and Methods: A total of forty patients, twenty with chronic periodontitis only with no CVD (Group A) and twenty with CVD and chronic periodontitis (Group B), were selected for the study. Clinical parameters including gingival index (GI), plaque index, gingival bleeding index, Pocket probing depth (PD), and clinical attachment level (CAL) were recorded. In addition, high-sensitivity CRP (hsCRP) levels were measured from the peripheral blood using turbidimetric immunoassay technique. Results: As compared to the patients in Group A, those in Group B had more severe periodontitis with greater CAL (6.02 ± 0.53 mm vs. 6.63 ± 0.85 mm, P = 0.009), probing pocket depth (PPD) (5.20 ± 0.31 mm vs. 5.73 ± 0.52 mm, P < 0.001), and GI score (2.25 ± 0.51 vs. 2.65 ± 0.76, P = 0.06). Group B patients also had significantly higher hsCRP levels (12.3 ± 8.84 mg/L vs. 2.28 ± 0.38 mg/L; P < 0.001). The hsCRP levels had a significant positive correlation with PPD and GI. Multivariate regression analysis showed that the presence of CVD was independently associated with elevated hsCRP levels in the study population. Conclusion: The present study shows that CVD is associated with more severe periodontitis which is reflected in higher hsCRP levels. In addition, elevated hsCRP showed an independent association with CVD, incremental to various periodontitis measures. These findings suggest that periodontitis may add to the inflammation burden of the individual, which may potentially increase inflammatory activity in atherosclerotic lesions and thus the risk for cardiovascular events.

The habitual level of physical activity of the human race has significantly and abruptly declined in the last few generations due to technological developments. The professional societies and government health agencies have published minimum physical activity requirement guidelines to educate the masses about the importance of exercise and to reduce cardiovascular (CV) and all-cause mortality at the population level. There is growing participation in marathon running by amateur, middle-aged cases with a belief that more intense exercise will give incremental health benefits. Experts have cautioned the nonathlete amateurs about the "exercise paradox" and probable deleterious effects of high-intensity prolonged exercise on CV and musculoskeletal system. The epidemiological studies suggest a "reverse J shaped" relationship between running intensity and CV mortality. The highest benefits of reduction in CV and all-cause mortality are achieved at a lower intensity of running while the benefits tend to get blunted at a higher intensity of running. The physicians should have a balanced discussion with the amateur runners training for a marathon, about risks and benefits of high-intensity exercise, and should evaluate them to rule out the occult coronary disease.

Low density lipoprotein cholesterol (LDL-C) is the target of lipid lowering therapy in subjects who have atherosclerotic cardiovascular disease (ASCVD) or who are at risk of developing it. There have been many debatable issues in this field. Should lifelong statins be prescribed for subjects at low risk of ASCVD in primary prevention? How low one can go in LDL-C lowering and is it safe? Should we "treat to target" or just administer high or moderate or low intensity statins based on the risk category? What is the role of nonstatin drugs in lipid lowering therapy? Are proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9 inhibitors) going to be the game changers? There is an abundance of literature looking at these matters. Statins continue to be the first choice in dyslipidemia management. PCSK9 inhibitors would be a welcome addition to the armamentarium or an attractive alternative in certain situations.

The role of blood components including platelets, in initiating inflammation, endothelial dysfunction, atherosclerosis, thrombus formation, thrombus growth, and acute vascular ischemic events, is well established. Given this recognized role played by platelets, there is a considerable interest in understanding the physiology and function of platelets, as well as in the development of novel platelet function-inhibitory drugs. The generation of the second messengers, calcium mobilization, shape change, adhesion, aggregation, contraction, release of granule contents, thrombus development, thrombus growth, and formation of hemostatic plug at the injured vessel surfaces, in brief, constitute platelet activation. Some of the known compounds that inhibit platelet activation include inhibitors of arachidonic metabolism (cyclooxygenase-1 inhibitors; aspirin, ibuprofen, etc.), adenosine diphosphate receptor antagonists (P2Y ₁₂ inhibitors), adenylyl and guanylyl cyclase stimulators, calcium antagonists, and GP11b/111a receptor antagonists. Since platelets have multiple mechanisms of achieving in vivo activation, it is difficult to design a novel drug that offers total protection for developing acute ischemic vascular events, without compromising coagulation mechanisms. Given this complexity, any aggressive antiplatelet therapy results in increased bleeding episodes. Having said that, we feel that there is a great window of opportunity for developing novel antiplatelet therapies. There is also scope for the development of fixed-dose combinations for the primary and secondary management of chronic diseases such as hypertension, heart disease, and type-2 diabetes.

The concept of "Yoga" is currently gaining a lot of popularity worldwide owing to its various health benefits and other advantages such as safety and ease of practice. There is considerable evidence accumulating related to its benefits on health, especially cardiovascular health. There is, however, a lot of confusion related to the term "Yoga" in the various studies as it comprises several different practices. More good quality studies are needed utilizing different components of "Yoga" investigating their effects on cardiovascular disease. There is also a change in the understanding of the role of the heart in the human body.

The science of pharmacovigilance (PV) is important to ensure safety of patients and healthy volunteers taking medicinal products. A number of stakeholders are involved who contribute to the success of this field of medicine. One such contributor is physicians and health-care professionals who work in different therapeutic areas such as cardiology. As the understanding of this science evolves, the role of cardiologist becomes even more vital. The process of developing drugs is getting more complex, time consuming, and costly. However, several efficiencies can be achieved around accelerated drug development, cost effectiveness, risk management, managing health authority expectations, and developing personalized medicines. This is possible by increased collaboration between cardiologists and pharmaceutical medicine professionals. Therefore, it is important for a cardiologist to understand the basics of the science of PV and contribute further bringing new safe medicines to patients.

Coronary vasospasm and myocarditis are both recognized mimics of ST elevation myocardial infarction with normal coronary arteries. The occurrence of both pathologies in the same patient has rarely been described. We report a case of a 27-year-old man initially presenting with history and electrocardiogram (ECG) findings consistent with acute myocarditis who subsequently developed severe chest pain and new ST elevation, mimicking a myocardial infarction. Subsequent coronary angiography was normal, indicative of coronary vasospasm being the cause of ECG changes and symptoms. Previous case reports with a similar presentation are reviewed and potential mechanisms causing this association discussed.