However, a recent study revealed that G6PD deficiency increases the cardiovascular risk up to 70%. The risk conferred by G6PD deficiency is moderate compared with the impact of primary cardiovascular risk factors. Besides, a published review hypothesized that G6PD deficiency  could reduce the antiplatelet efficacy of clopidogrel (clopidogrel resistance). Epidemiology
G6PD deficiency is the second most common human enzyme defect after ALDH2 deficiency, being present in more than 400 million people worldwide. G6PD deficiency resulted in 4,100 deaths in 2013 and 3,400 deaths in 1990. African, Middle Eastern and South Asian people are affected the most, including those who have these ancestries. A side effect of this disease is that it confers protection against malaria, in particular the form of malaria caused by Plasmodium falciparum, the most deadly form of malaria. A similar relationship exists between malaria and sickle-cell disease. One theory to explain this is that cells infected with the Plasmodium parasite are cleared more rapidly by the spleen. This phenomenon might give G6PD deficiency carriers an evolutionary advantage by increasing their fitness in malarial endemic environments. In vitro studies have shown that the Plasmodium falciparum is very sensitive to oxidative damage. This is the basis for another theory, that is that the genetic defect confers resistance due to the fact that the G6PD-deficient host has a higher level of oxidative agents that, while generally tolerable by the host, are deadly to the parasite. History
The modern understanding of the condition began with the analysis of patients who exhibited sensitivity to primaquine.
The small Q-waves that are usually seen in the lateral leads are absent in LBBB. T-waves usually point in the opposite direction to the terminal portion of the preceding QRS - positive QRS complexes have negative T-waves while negative QRS complexes have positive T-waves. The ST segments typically slur into the T-wave and often appear elevated in leads with negative QRS complexes. The axis may be normal but may be deviated to the left or right.There are also partial blocks of the left bundle branch: "left anterior fascicular block" (LAFB) and a "left posterior fascicular block" (LPFB). This refers to the block after the bifurcation of the left bundle branch. Diagnostic consequences
The presence of LBBB results in that electrocardiography (ECG) cannot be used to diagnose left ventricular hypertrophy or Q wave infarction, because LBBB in itself results in widened QRS complex, and changes in the ST segment consistent with ischemia or injury. Treatment
Patients with LBBB require complete cardiac evaluation, and those with LBBB and syncope or near-syncope may require a pacemaker. Some patients with LBBB, a markedly prolonged QRS (usually > 150 ms), and systolic heart failure may benefit from a biventricular pacemaker, which allows for better synchrony of heart contractions. See also
Bundle branch block
Right bundle branch block
Sgarbossas criteria

References


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